CANCER SCIENCE
·
2023
·
IF 5.7
Bo‐Wen Zuo,Wan‐Xin Yao,Meng‐Die Fang,Juan Ren,Ling‐Lan Tu,Run‐Jie Fan,Yan‐Mei Zhang
The Brother of Regulator of Imprinted Sites (BORIS, gene symbol CTCFL) has previously been shown to promote colorectal cancer cell proliferation, inhibit cancer cell apoptosis, and resist chemotherapy. However, it is unknown whether Boris plays a role in the progression of in situ colorectal cancer. Here Boris knockout (KO) mice were constructed. The function loss of the cloned Boris mutation that was retained in KO mice was verified by testing its activities in colorectal cell lines compared with the Boris wild‐type gene. Boris knockout reduced the incidence and severity of azoxymethane/dextran sulfate‐sodium (AOM/DSS)‐induced colon cancer. The importance of Boris is emphasized in the progression of in situ colorectal cancer. Boris knockout significantly promoted the phosphorylation of γH2AX and the DNA damage in colorectal cancer tissues and suppressed Wnt and MAPK pathways that are responsible for the callback of DNA damage repair. This indicates the strong inhibition of colorectal cancer in Boris KO mice. By considering that the DSS‐promoted inflammation contributes to tumorigenesis, Boris KO mice were also studied in DSS‐induced colitis. Our data showed that Boris knockout alleviated DSS‐induced colitis and that Boris knockdown inhibited the NF‐κB signaling pathway in RAW264.7 cells. Therefore Boris knockout eliminates colorectal cancer generation by inhibiting DNA damage repair in cancer cells and relieving inflammation in macrophages. Our findings demonstrate the importance of Boris in the development of in situ colorectal cancer and provide evidence for the feasibility of colorectal cancer therapy on Boris.
研究领域:
癌症生物学
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分子生物学
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免疫学
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遗传学
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DOI
PubMed
高影响因子
Oncology Letters
·
2021
·Vol. 21
·期 3
·1-1
·
IF 2.967
Jiaxue Hao,Xufen Dai,Juan Gao,Yuexuan Li,Zhaoling Hou,Zhongman Chang,Yuxin Wang
Colorectal cancer (CRC) is the third most common cancer worldwide, with high incidence and mortality rates. Conventional therapies, including surgery, chemotherapy and radiation, are extensively used for the treatment of CRC. However, patients present with adverse effects, such as toxicity, hepatic injury and drug resistance. Thus, there is an urgent requirement to identify effective and safe therapy for CRC. Curcumin (CUR), a polyphenol substrate extracted from the rhizome of Curcuma longa, has been extensively studied for the treatment of CRC due to its high efficacy and fewer side effects. Previous studies have reported that several signaling pathways, such as NF‑κB, Wnt/β‑catenin, are involved in the antitumor effects of CUR in vitro. However, the effect and mechanisms in vivo are not yet fully understood. The present study aimed to determine the molecular mechanism of colorectal cancer in vivo. Reverse transcription‑quantitative PCR, western blot and immunohistochemistry analyses were performed to determine the underlying molecular mechanism of curcumin's anti‑cancer effect in azoxymethane‑dextran sodium sulfate induced colorectal cancer. The results of the present study demonstrated that CUR suppressed tumorigenesis in AOM‑DSS induced CRC in mice, and anticancer effects were exerted by suppressing the expression of pro‑inflammatory cytokines, and downregulating Axin2 in the Wnt/β‑catenin signaling pathway. Taken together, these results exhibit the potential in vivo mechanisms of the anticancer effects of CUR, and highlight Axin2 as a potential therapeutic target for CRC.
研究领域:
肿瘤学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
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2026
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IF 5.1
Yinyue Wang,Ruyi Zhang,Yangjiao Xu,Hongtao Shi,Xueyao Hu,Nairong Yu,Yu-Qiang Zhao,Baomin Fan,Guangzhi Zeng
NCTD-01 shows anti-inflammatory and cytotoxic effects in vitro and in vivo. • NCTD-01 exhibits low in vivo toxicity and a high oral MTD. • NCTD-01 suppresses AOM/DSS-induced colorectal cancer safely in mice. • NCTD-01 limits inflammation-to-cancer transition via NF-κB and Treg regulation. Although cantharidin (CTD) exhibits significant clinical efficacy against various cancers, its clinical utility is severely hampered by profound systemic toxicity. Thus, structural modification of CTD to obtain analogues with potent anticancer activity and lower toxicity is essential for advancing CTD-based therapeutics. Building on our previous synthesis of a series of C-5 alkynyl-substituted CTD analogues with potent anti-inflammatory properties, this study investigates the anticancer potential of a new analogue NCTD-01 demonstrated a favorable safety profile in mice, with the maximum tolerated dose (MTD) for oral administration exceeding 1852 mg/kg. In addition to exhibiting potent in vitro and in vivo anti-inflammatory activities comparable to its analogues, NCTD-01 displayed cytotoxicity against colon cancer cell lines and exhibited therapeutic efficacy in an azoxymethane/dextran sulfate sodium-induced orthotopic mouse model of colorectal cancer. Molecular analyses revealed that NCTD-01 reduced Ki-67 expression, suppressed the mRNA levels of pro-inflammatory and immunosuppressive mediators ( IL-1β , COX-2 , IL-6 , IL-10 , and TGF-β ) in colonic tumor tissues, and decreased serum levels of TNF-α and IL-1β. Furthermore, NCTD-01 treatment led to reduced expression of Foxp3, CD25, PD-1, and PD-L1, alongside enhanced CD8 and GITR expression in colorectal tissues, suggesting an effective modulation of tumor-associated immune responses. This study suggests that NCTD-01, a new C-5 alkynyl-substituted CTD analogue, may help alleviate the inflammation-to-cancer transition through tumor-associated immune modulation while maintaining a favorable safety profile, pointing to its potential as a candidate for anticancer drug discovery. Download: Download high-res image (99KB) Download: Download full-size image
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DOI
高影响因子
Probiotics and Antimicrobial Proteins
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2024
·Vol. 17
·期 3
·1523-1535
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IF 4.4
Wang Minyu,Gao Chongzheng,Lessing Duncan James,Chu Weihua
Colorectal cancer is the third most common cancer in the world today, and studies have shown that the ratio of Candida to Saccharomyces cerevisiae increased, and the abundance of S. cerevisiae in the intestines of patients with colorectal cancer decreased, which suggests that there is an imbalance in the proportion of fungi in the intestines of patients with colorectal cancer. The objective of this study was to screen S. cerevisiae isolate from traditional Chinese fermentation starters and assess its ability to ameliorate dysbiosis and to alleviate the carcinogenic process of azoxymethane/dextran sodium sulfate–induced colorectal cancer in mice model. S. cerevisiae strain SC-2201 was isolated and exhibited probiotic properties, including the ability to survive in an acidic pH environment and in the presence of bile salts in the gastrointestinal tract, as well as antioxidant activities. Oral administration of S. cerevisiae SC-2201 not only alleviated weight loss but also reduced colonic shortening and histological damage in azoxymethane/dextran sodium sulfate–induced colorectal cancer in mice. Furthermore, the administration of S. cerevisiae SC-2201 suppressed the expression of proinflammatory mediators, such as interleukin-1β, interleukin-6, cyclooxygenase-2, vascular endothelial growth factor, nucleotide-binding domain, leucine-rich repeat, and pyrin domain–containing protein 3. Specifically, the analysis of gut bacteriome showed a significant decrease in Bacteroidota and Campylobacterota levels, as well as an increase in Proteobacteria level in the colorectal cancer group, which was alleviated by supplementation with S. cerevisiae SC-2201. The analysis of the mycobiome revealed a significant increase in the levels of Basidiomycota , Apiosordaria , Naganishia , and Taphrina genera in the colorectal cancer group, which were alleviated after supplementation with S. cerevisiae SC-2201. However, the levels of Xenoramularia , Entoloma , and Keissleriella were significantly increased after administration with S. cerevisiae SC-2201. Overall, the findings of this study demonstrate that S. cerevisiae SC-2201 possesses potential probiotic properties and can effectively attenuate the development of colorectal cancer, highlighting its cancer-preventive potential. This is the first report of a S. cerevisiae strain isolated from traditional Chinese fermentation starters which showed good probiotic properties, and mitigated azoxymethane/dextran sodium sulfate–induced colorectal cancer by modulating the gut microbiome and blocking proinflammatory mediators in mice.
研究领域:
微生物学
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肿瘤学
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免疫学
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胃肠病学
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分子生物学
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药理学
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DOI
高影响因子
Food Bioscience
·
2025
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IF 5.9
Yutong Ma,Jiaxi Li,Shuyu Liu,Wenlong Yu,Yaxin Sang,Xianghong Wang
Sulforaphane (SFN), a bioactive compound derived from cruciferous vegetables, exhibits chemopreventive properties agains various malignancies. Colitis-associated colorectal cancer (CAC) is a malignancy that develops through chronic inflammation-driven carcinogenesis in patients with long-standing inflammatory bowel disease. This study demonstrates a novel mechanism by which SFN protects against CAC through the simultaneous regulation of the Wnt/β-catenin signaling pathway and gut microbiota. Using an azoxymethane(AOM)/dextran sulfate salt sodium(DSS)-induced CAC mouse model to systematically evaluate SFN's therapeutic potential. Comprehensive assessments included histopathological examination, molecular analysis of inflammatory cytokines and proliferation markers, 16S rDNA sequencing for gut microbiota characterization, short-chain fatty acid (SCFA) profiling, and mechanistic investigation of Wnt/β-catenin pathway components. The experimental results showed that SFN intervention significantly alleviated clinical symptoms in mice, reduced inflammatory cytokine levels (IFN-γ, interferon-gamma; IHC, immune histochemical; IL-17, interleukin-17; IL-6, interleukin-6; MPO, myeloperoxidase) and suppressed proliferation markers (PCNA, proliferating cell nuclear antigen, antigen identified by monoclonal antibody Ki-67, Ki-67). Notably, SFN administration significantly restored the levels of major SCFAs, including acetate, propionate, and butyrate, which were markedly reduced in CAC mice. Mechanistically, SFN inhibited the Wnt/β-catenin signaling pathway by down-regulating the expression of β-catenin, cyclin D1 and c-myc expression. Concurrently, SFN restored gut microbial diversity, increased beneficial bacteria, and reduced pathogenic genera. The observed increase in SCFAs levels was correlated with these microbial improvements, and orrelation analysis further linked these microbial shifts to clinical improvements. Our findings reveal that SFN mitigates CAC progression by coordinated modulation of both Wnt/β-catenin signaling and gut microbiota, with the restoration of SCFAs production representing a key functional outcome, highlighting its potential as a multi-target dietary intervention for colorectal cancer prevention.
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高影响因子
Gut Microbes
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2025
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IF 11
Yong Sun,Qiwen Wang,Yao Jiang,Jiamin He,Dingjiacheng Jia,Man Luo,Wentao Shen,Qingyi Wang,Yadong Qi,Yifeng Lin,Ying Zhang,Lan Wang,Liangjing Wang,Shujie Chen,Lina Fan
Gut microbes play a crucial role in regulating the tumor microenvironment (TME) of colorectal cancer (CRC). Nevertheless, the deep mechanism between the microbiota-TME interaction has not been well explored. In this study, we for the first time discovered that Lactobacillus intestinalis (L. intestinalis) effectively suppressed tumor growth both in the AOM/DSS-induced CRC model and the ApcMin/+ spontaneous adenoma model. Our investigation revealed that L. intestinalis increased the infiltration of immune cells, particularly dendritic cells (DC), in the TME. Mechanically, the tumor-derived CCL5 induced by L. intestinalis recruited DC chemotaxis through the NOD1/NF-κB signaling pathway. In clinical samples and datasets, we found positive correlation between L. intestinalis, CCL5 level, and the DC-related genes. Our study provided a new strategy for microbial intervention for CRC and deepened the understanding of the interaction between tumor cells and the immune microenvironment modulated by gut microbes.
研究领域:
肿瘤学
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微生物学
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免疫学
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DOI
PubMed
高影响因子
Food & Function
·
2020
·Vol. 11
·期 9
·8259-8272
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IF 4.171
Shuhua Shan,Yue Xie,Chengying Zhang,Bin Jia,Hanqing Li,Zhuoyu Li
Homology of medicine and food-zizyphi spinosi semen (ZSS) exhibits abundant pharmacological activities, such as sedation, hypnosis and anti-depression. In the present study, the water soluble polyphenols extracted from ZSS via the acid digestion method were named ZSSP, and exhibited significant anti-colorectal cancer (CRC) activity, characterized by restraining cell proliferation, promoting cell apoptosis and increasing chemo-sensitivity of CRC cells. The potential of ZSSP in vivo was further evaluated in an AOM/DSS-induced colitis-associated carcinogenesis (CAC) mouse model. Intriguingly, ZSSP diminished the number and volume of CAC polyps in mice in a dose-dependent manner, and effectively limited the damage of mice organs induced by AOM/DSS. The immunohistochemistry result showed that the elevated CRC early markers in CAC mice, such as COX-II, EMR1, and Ki67, were potently prevented by the ZSSP treatment. Further, the component in ZSSP with the anti-CRC activity was identified as spinosin by the macroporous resin of SP207 and RP-HPLC-MS/MS. Interestingly, during the extraction process, sodium ions were introduced forming spinosin·Na+, which had better water solubility and more remarkable anti-CRC activity than the spinosin. This study provides a new pharmacological property of spinosin derived from ZSS, inhibiting the growth of human CRC cells and colitis-associated CRC in mice, which indicates its potential use as a natural agent against CRC.
研究领域:
肿瘤学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Jingya Ruan,Huimin Li,Mengqi Lu,Mimi Hao,Fan Sun,Haiyang Yu,Yi Zhang,Tao Wang
Background Jujube, a popular fruit from the Rhamnaceae family, relieves colorectal inflammation caused by spleen deficiency and has been used in many formulas in clinical for decades to treat colorectal cancer (CRC). As of yet, the therapeutic substances and mechanism of their action are unknown. Purpose The purpose of this study is to define the therapeutic substances of jujube and its mechanism of action in treating CRC . Methods The pharmacological effects of jujube extract and its fractions were evaluated in vivo using a CRC mouse model induced by AOM/DSS. The DAI value, colon length, mortality, tumor burden, and histological tumor size of the treated animals were compared. To explore the potential therapeutic substances, LC-MS analysis was conducted to characterize the serum migration components. A network pharmacology experiment was carried out for potential molecular targets. To verify the therapeutic substances as well as the molecular mechanism of jujube intervening CRC, cellular MTT assay of the serum migration components, Western blot and IHC tests were conducted. Results The in vivo pharmacological studies showed that compared to AOM/DSS treated mice, the mortality and DAI value, tumor burden, and histological tumor size of jujube extract and its fat-soluble fraction (mainly contained triterpenes) treated mice were significantly reduced, and their colon lengths were obviously longer than AOM/DSS treated mice. The targeted-LC/MS analysis supposed triterpenes 3, 7, 9, 11, 12, 14, 17 – 21, and 25 – 28 to be the serum migration components, which might be the potential therapeutic substances. In the network pharmacology experiment, the GO annotation and enrichment analysis of the KEGG pathway indicated that PI3K-Akt pathway and inflammatory reaction were important factors for jujube inhibiting CRC. Cellular MTT assay of serum migration components indicated that the potential effective substances from fat-soluble fraction to be triterpenes 3, 7, 17, 19, 20, and 25. The Western blot and IHC assays implied that the jujube extract, its fat-soluble fraction, and triterpenes 7, 17, and 20 showed inhibition on the expression of PI3K/Akt/NF-κB signaling pathway-related proteins. Additionally, it was noted in the pharmacodynamic experiment that ZJL's effectiveness was more apparent than ZJH and SQL in tumor burden rate, colon length, and spleen weight, which indicated that the efficacy of ZJ is contributed from CD and SQ, and they may have a synergistic effect on anti-CRC. Conclusion These results for the first time provide evidence that jujube triterpenes possess an anti-CRC effect, their mechanism was involving the control of the PI3K/Akt/NF-κB signaling pathway. What's more, the potential synergistic effect of the fat-soluble and water-soluble components found in this study provided a solid foundation for our deep understanding of how jujube can ameliorate CRC.
研究领域:
药理学
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肿瘤学
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分子生物学
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中医药
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DOI
PubMed
高影响因子
Nutrients
·
2026
·Vol. 18
·期 2
·310
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IF 5
Xin Zhang,Di Wang,Yang Wang,Meimei Wang,Juncheng Wang,Yue Sun,Siman Chen,Xinting Qu,Antong Xia,Hongxin Liu,Jihui Wang,Meng Liu
(E)-Flavokawain A (FKA), the primary chalcone constituent of Piper methysticum , exhibits diverse pharmacological properties and holds significant potential for therapeutic development. Objectives : This study aims to investigate the anti-colorectal cancer effects and mechanisms of FKA. Methods : Using AOM/DSS-induced colorectal cancer models in C57 mice, the research examines the impact of different FKA doses, employing 16S rRNA and metabolomics to explore the potential mechanism. Results : The findings indicated that FKA significantly inhibited the progression of colorectal cancer in C57 mice by modulating the composition of the gut microbiota. This modulation involved the suppression of endotoxin secretion by pathogenic bacteria and the concurrent augmentation of beneficial bacteria. Furthermore, in the context of metabolic pathways, FKA regulates lipid metabolism and arachidonic acid metabolism, thereby mitigating the inflammatory transformation associated with colorectal cancer. Conclusions : These findings provide valuable insights supporting the potential of FKA as a viable preventive strategy against CRC.
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PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2023
·
IF 5.8
Xiangli He,Jiayan Cui,Hui Ma,Naijipu Abuduaini,Ying Huang,Lu Tang,Wanyan Wang,Yuanyuan Zhang,Yang Wang,Weiqiang Lu,Bo Feng,Jin Huang
Inosine monophosphate dehydrogenase (IMPDH) catalyzes the rate-limiting reaction in the de novo synthesis pathway of guanine nucleotides that is highly required for cancer cell outgrowth. Herein, we found that IMPDH isoform 2 (IMPDH2) is highly expressed in colorectal cancer (CRC) and is correlated with poor patient prognosis. Via structure-based virtual screening, we identified berberrubine, a critical ingredient of the medical plant Coptis chinensis, as a novel, selective, and competitive inhibitor of IMPDH2, which demonstrated over 15-fold selectivity to IMPDH2 than IMPDH1. Besides, we also confirmed the interaction between berberrubine and IMPDH2. Of note, berberrubine treatment significantly impairs the growth of human CRC cells in a dose-dependent manner, which can be rescued by supplementing with guanosine. Furthermore, oral administration of berberrubine remarkably reduced tumor volume and weight in a human cell line-derived xenograft model. Importantly, the anti-cancer activity of berberrubine was also confirmed by using the azoxymethane (AOM) / dextran sulfate sodium (DSS)-induced spontaneous CRC mouse model. Taken together, our study highlights that berberrubine acts as a novel IMPDH2 inhibitor, suppressing the growth of CRC in vitro and in vivo , providing a fresh perspective for its potential application in the treatment of CRC.
研究领域:
肿瘤学
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药理学
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分子生物学
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癌症生物学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Xin Liu,Chunli Yan,Chunxiao Chang,Fansong Meng,Wenjie Shen,Song Wang,Yi Zhang
Background Mycotoxins, such as aflatoxin and ochratoxin A (OTA), are found at measurable levels in many staple foods; the health implications of long-term exposure of such toxins are poorly understood. Increasing evidence has confirmed the important role of OTA in upregulation of oxidative stress- and inflammatory response-induced tissue injury. However, it remains unknown whether ochratoxin A can promote chronic colitis and its associated colon cancer (CRC) development, and potential molecular mechanism. Additionally, RING finger-interacting protein with C kinase (RINCK) is a ubiquitin ligase and mediates immune response. Unfortunately, the potential molecular function of RINCK on regulation of colitis is still largely unknown. Purpose This study aims to provide mechanistic evidence that the role of RINCK in colitis and early colorectal cancer progression in response to OTA treatment via targeting nuclear factor erythroid 2-related factor 2 (NRF2). Methods The Cancer Genome Atlas (TCGA) database, GEO database, human subjects with CC phenotype and CC cell lines were used in this work. Pathological links between OTA, RINCK and treatment of CC are revealed through comprehensive means such as biological information analysis, clinical experiments, RNA-seq, and verification experiments. Results In this study, under oxidative stress in setting of colitis, we first identified RINCK as a key regulatory factor and a novel endogenous suppressor of nuclear factor erythroid 2-related factor 2 (NRF2), and we also confirm that RINCK is a NRF2 partner protein that catalyses its ubiquitination and degradation in intestinal epithelial cells (IECs). Notably, in vivo study, pathological phenotypes triggered by OTA pretreatment, accompanied by post-treatment of dextran sulfate sodium (DSS)-induced colitis was significantly mitigated by IEC-specific deficiency of Rinck , IEC- Rinck (KO) and adenovirus-associated virus (AAV)-triggered suppression of Rinck in rodent model, and lentivirus (LV)-mediated downregulation of Rinck (LV-sh Rinck ) in rabbit model, as determined by decreased endogenous reactive oxygen species (ROS) production, pro-inflammatory cytokines contents, improved body weights, reduced survival rates, restored colon length, assuasive DAI and histological scores. Inversely, transgenic mice by IEC-specific Rinck overexpression, IEC- Rinck (OE) accelerated colitis in acute or chronic colitis rodent models and in vitro experiments. Moreover, we found that OTA pretreatment-promoted azoxymethane (AOM)/DSS-induced colitis-associated early colorectal cancer (CRC) was also dramatically reduced by IEC- Rinck (KO), indicated by the decreased tumor number and corresponding KI-67 levels. Clinical samples analysis revealed that RINCK levels were greatly increased in tumor tissues of patients with CRC phenotypes. In parallel, RINCK deletion remarkably retarded the proliferation of colon cancer and tumor growth in vitro and in vivo , respectively. Mechanistically, in response to onset of colitis, RINCK directly interacts with NRF2 and promotes ubiquitin-proteasome degradation via increasing K48-linkage ubiquitin chain, thus leads in suppression of NRF2 nuclear translocation and its downstream cascade inactivation, which retards antioxidant defense. Conclusion The findings suggested that oral sub-chronic exposure of OTA significantly facilitates DSS-induced colitis and colitis-associated CRC development. These results further elucidated the potential role of RINCK in colitis progression by mediating NRF2 degradation, and could be considered as a therapeutic target for the treatment of such disease.
研究领域:
毒理学
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免疫学
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癌症生物学
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分子生物学
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胃肠病学
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DOI
PubMed
高影响因子
Science China-Life Sciences
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2024
·
IF 8
Zhang Yinghui,Liu Yadan,Jiang Bing,Chen Lifan,Hu Jie,Niu Buying,Chang Jie,Fan Zisheng,Zhou Jingyi,Wang Yajie,Teng Dan,Ma Ning,Wang Xiaofeng,Yang Ruirui,Zheng Mingyue,Zhang Sulin
The development of STING inhibitors for the treatment of STING-related inflammatory diseases continues to encounter significant challenges. The activation of STING is a multi-step process that includes binding with cGAMP, self-oligomerization, and translocation from the endoplasmic reticulum to the Golgi apparatus, ultimately inducing the expression of IRF3 and NF-κB-mediated interferons and inflammatory cytokines. It has been demonstrated that disruption of any of these steps can effectively inhibit STING activation. Traditional structure-based drug screening methodologies generally focus on specific binding sites. In this study, a TransformerCPI model based on protein primary sequences and independent of binding sites is employed to identify compounds capable of binding to the STING protein. The natural product Licochalcone D (LicoD) is identified as a potent and selective STING inhibitor. LicoD does not bind to the classical ligand-binding pocket; instead, it covalently modifies the Cys148 residue of STING. This modification inhibits STING oligomerization, consequently suppressing the recruitment of TBK1 and the nuclear translocation of IRF3 and NF-κB. LicoD treatment ameliorates the inflammatory phenotype in Trex1 −1− mice and inhibits the progression of DSS-induced colitis and AOM/DSS-induced colitis-associated colon cancer (CAC). In summary, this study reveals the potential of LicoD in treating STING-driven inflammatory diseases. It also demonstrates the utility of the TransformerCPI model in discovering allosteric compounds beyond the conventional binding pockets.
研究领域:
免疫学
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药理学
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分子生物学
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炎症
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药物发现
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）