Bioengineered
·
2021
·
IF 3.269
Yan Wang,Zhiqiang Cheng,Jing Xu,Meina Lai,Liming Liu,Min Zuo,Lin Dang
Excessive activation of signal transducer and activator of transcription 3 (STAT3) is implicated in breast cancer (BC) chemoresistance, but its underlying mechanism is not fully understood. There are STAT3 binding sites in fat mass and obesity-associated protein (FTO) promoter region, thus STAT3 may regulate the transcription of FTO. This study aimed to investigate the correlation between FTO and STAT3 in BC chemoresistance. Herein, FTO and STAT3 were highly expressed in doxorubicin-resistant BC (BC-DoxR) cells. CHIP assay verified the binding between STAT3 and FTO promoter in BC-DoxR cells. Dual luciferase reporter assay showed that FTO promoter activity was inhibited by S3I-201 (STAT3 inhibitor) but enhanced by epidermal growth factor (EGF, STAT3 activator) in BC-DoxR and BC cells. FTO mRNA and protein expression were suppressed by S3I-201 in BC-DoxR cells and EGF-stimulated BC cells. Notably, FTO regulated total N6-methyladenosine (m6A) levels in BC-DoxR and BC cells but could not affect STAT3 mRNA expression, indicating that FTO was not involved in the m6A modification of STAT3. However, FTO could activate STAT3 signaling in BC-DoxR and BC cells. Besides, FTO knockdown inhibited the doxorubicin resistance of BC-DoxR cells, while FTO overexpression enhanced the doxorubicin resistance and weakened the doxorubicin sensitivity of BC cells. Moreover, decreased doxorubicin resistance by STAT3 knockdown was abolished by FTO overexpression and decreased doxorubicin sensitivity by STAT3 overexpression was reversed by FTO knockdown, indicating that FTO was implicated in STAT3-mediated doxorubicin resistance and impairment of doxorubicin sensitivity of BC cells. Altogether, our findings provide a mechanism underlying BC doxorubicin resistance.
研究领域:
肿瘤学
·
分子生物学
·
癌症生物学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2018
·
IF 3.616
Qiaozhu Tan,Ming Zhang,Lujing Geng,Zhenghua Xia,Cen Li,Muhammad Usman,Yuzhi Du,Lixin Wei,Hongtao Bi
Methylmercury (MeHg + ) is an extremely toxic organomercury cation that can induce severe neurological damage. Once it enters the body, methylmercury binds to amino acids or proteins containing free sulfhydryl groups. In particular, methylmercury is known to bind with human serum albumin (HSA) in human plasma; however, the effects of methylmercury-HSA conjugate (MeHg-HSA) on the central nervous system (CNS) are not fully understood. In the present study, we used the microglial cell line N9 as the target cells to evaluate the effect of MeHg-HSA on physiological function of the CNS preliminarily. The various factors in the cell culture were monitored by MTT assay, total lactate dehydrogenase assay, ELISA , qPCR, Western blot and flow cytometry techniques. The results showed that low-dose treatment with MeHg-HSA activated N9 cells, promoting cell proliferation and total cell number, enhancing NO and intracellular Ca 2+ levels, and suppressing the release of TNFα and IL1β without cytotoxic effects; while high-dose MeHg-HSA exhibited cytotoxic effects on N9 cells, including promoting cell death and increasing the secretion of TNFα and IL1β. These results indicate that MeHg-HSA causes hormesis in microglia N9 cells. Furthermore, ERK/MAPKs and STAT3 signaling pathways related to the hormesis of MeHg-HSA on N9 cells. In addition, low dose of MeHg-HSA might be viewed as something very close to a lowest observed adverse effect level (LOAEL) for N9 cells. These findings will be useful for investigating the hormesis mechanism of MeHg + and exploring the specific functions of MeHg-sulfhydryl conjugates on the central nervous system.
研究领域:
神经毒理学
·
细胞生物学
·
药理学
·
毒理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2023
·
IF 5.2
Yanping Fan,Meilan Xue,Tianhu Shan,Yixian Bai,Huaqi Zhang,Man Liu,Peng Wang,Xi Liang,Hui Liang
Alcoholic liver fibrosis (ALF) is a reversible pathological change in the liver caused by chronic alcohol consumption and is associated with the activation of hepatic stellate cells . Recent findings suggest that niacin can lower triglyceride levels and exert potent antioxidant effects in liver damage. However, the therapeutic effects and molecular mechanisms of niacin in liver fibrosis remain unclear. Therefore, this study aimed to investigate the effects and mechanisms of niacin in ALF using in vivo and in vitro experiments. To establish a murine model of ALF, male C57BL/6N mice were fed a Lieber–DeCarli liquid diet containing 4 % (vol/vol) ethanol and injected with carbon tetrachloride twice weekly (2 mL/kg) for 8 weeks. L-02 and LX2 cells were treated with 400 μM acetaldehyde for 24 h to establish an in vitro ALF model. Serum parameters were examined to investigate the protective effects of niacin against ALF, and network pharmacology was used to identify potential targets and pathways of niacin. Niacin protects against ALF by suppressing the serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase , and alkaline phosphatase . Additionally, niacin treatment ameliorated liver fibrosis by improving the antioxidant system, inhibiting heat shock protein 90 (HSP90) activation, promoting signal transducer and activator of transcription 3 (STAT3) ubiquitination , and suppressing the JAK1/STAT3 signaling pathway . Collectively, this study provides experimental evidence that niacin protects against ALF by downregulating the HSP90/JAK1/STAT3 signaling pathway.
研究领域:
药理学
·
肝病学
·
分子生物学
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细胞生物学
✓ 已验证
产品关联
DOI
高影响因子
International Journal of Biological Sciences
·
2021
·
IF 6.582
Yadong Liu,Huiyan Lv,Xingyi Li,Jiannan Liu,Song Chen,Yaodong Chen,Yinshan Jin,Ruihua An,Shiliang Yu,Zhigang Wang
Of all pathological types of renal cell cancer (RCC), clear cell renal cell carcinoma (ccRCC) has the highest incidence. Cyclovirobuxine (CVB), a triterpenoid alkaloid isolated from Buxus microphylla , exhibits antitumour activity against gastric cancer and breast cancer; however, the mechanism by which CVB inhibits ccRCC remains unclear. The aim of our study was to explore the antitumour effects of CVB on ccRCC and to elucidate its exact mechanism. Cell viability, proliferation, cell cycle distribution, apoptosis, wound healing and invasion were evaluated. Furthermore, Western blotting, immunofluorescence staining, immunohistochemical staining, and bioinformatics analyses were utilized to comprehensively probe the molecular mechanisms. The in vivo curative effect of CVB was explored using a 786-O xenograft model established in nude mice. CVB reduced cell viability, proliferation, angiogenesis, the epithelial-mesenchymal transition (EMT), migration and invasion. In addition, CVB induced cell cycle arrest in S phase and promoted apoptosis. The expression of the EMT-related transcription factor Snail was significantly downregulated by CVB via the inhibition of the AKT, STAT3 and MAPK pathways. We revealed that insulin-like growth factor binding protein 3 (IGFBP3) was the true therapeutic target of CVB. CVB exerted anti-ccRCC effects by blocking the IGFBP3-AKT/STAT3/MAPK-Snail pathway. Targeted inhibition of IGFBP3 with CVB treatment may become a promising therapeutic regimen for ccRCC.
研究领域:
肿瘤学
·
分子生物学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
DRUG DEVELOPMENT RESEARCH
·
2023
·Vol. 84
·期 3
·582-600
·
IF 3.8
Jiabin Zhou,Yuhan Liu,Jun Chen,Nanxiang Xiong,Dongye Yi
Kaempferol (Kae) is a natural flavonoid that has multiple biological activities, such as anti-inflammatory and antitumor activities. However, few studies have been reported on antiglioma effects of Kae. This study aimed to explore the effects and potential mechanisms of Kae and synergistic antitumor activities with gefitinib (Gef) on glioma. Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays were used to detect cytotoxicity and cell proliferation. Cell apoptosis and the cell cycle were detected by flow cytometry. Transwell assays were used to detect the migratory and invasive abilities of glioma cells. Network pharmacology and molecular docking analysis were used to screen for core targets of Kae in glioma therapy. Xenograft tumor nude mice were established with U251 cells to verify the antiglioma effects of Kae in vivo. A terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to detect apoptosis in tumor tissues. The expression of proteins was detected by immunohistochemistry and western blot analysis. Kae inhibited cell proliferation, promoted apoptosis, and induced cell cycle arrest in the G2/M phase of glioma cells in a concentration-dependent manner. Kae inhibited the migration and invasion of glioma cells at low concentrations. Network pharmacology analyses showed that epidermal growth factor receptor (EGFR) and SRC proto-oncogene (SRC) might be direct molecular-binding targets of Kae. Our results showed that Kae inhibited the levels of phosphorylated EGFR, phosphorylated SRC (p-SRC), and phosphorylated signal transducer and activator of transcription 3 (STAT3). In addition, the combination of Kae with Gef significantly inhibited the proliferation of glioma cells. Kae further inhibited EGFR phosphorylation after treatment with Gef. Similarly, Kae further enhanced the inhibition of p-SRC caused by SU6656. Finally, we demonstrated that Kae exerted great antitumor activities and enhanced the antitumor effect of Gef by inhibiting EGFR/SRC/STAT3 signaling pathway in vivo. Kae played a potential role and synergistic antiglioma effects with Gef by inhibiting the phosphorylation of EGFR/SRC dual targets. Kae is expected to be a candidate drug or chemosensitizer in glioma therapy.
研究领域:
肿瘤学
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药理学
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分子生物学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2022
·Vol. 23
·期 18
·10887
·
IF 6.208
Jing Jie,Guomu Liu,Jingyue Feng,Desheng Huo,Yixuan Wu,Hongyan Yuan,Guixiang Tai,Weihua Ni
Our previous study found that CpG oligodeoxynucleotides 1826 (CpG 1826), combined with mucin 1 (MUC1)-maltose-binding protein (MBP) (M-M), had certain antitumor activity. However, this combination is less than ideal for tumor suppression (tumors vary in size and vary widely among individuals), with a drawback being that CpG 1826 is unstable. To solve these problems, here, we evaluate MF59/CpG 1826 as a compound adjuvant with M-M vaccine on immune response, tumor suppression and survival. The results showed that MF59 could promote the CpG 1826/M-M vaccine-induced tumor growth inhibition and a Th1-prone cellular immune response, as well as reduce the individual differences of tumor growth and prolonged prophylactic and therapeutic mouse survival. Further research showed that MF59 promotes the maturation of DCs stimulated by CpG1826/M-M, resulting in Th1 polarization. The possible mechanism is speculated to be that MF59 could significantly prolong the retention time of CpG 1826, or the combination of CpG 1826 and M-M, as well as downregulate IL-6/STAT3 involved in MF59 combined CpG 1826-induced dendritic cell maturation. This study clarifies the utility of MF59/CpG 1826 as a vaccine compound adjuvant, laying the theoretical basis for the development of a novel M-M vaccine.Keywords:MF59;CpG 1826;compound adjuvant;tumor vaccine;MUC1-MBP;dendritic cells
研究领域:
免疫学
·
肿瘤学
·
疫苗学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
·
2024
·
IF 6.1
Taiping Li,Yougang Zhang,Rong Dong,Wenjie Bi,Songsong Wang,Kewu Zeng,Liwen Han
American ginseng (AG) has been reported to have anti-inflammatory effects in many diseases, but the key molecules and mechanisms are unclear. This study aims to evaluate the anti-inflammatory mechanism of AG and identify the key molecules by in vivo and in vitro models. Zebrafish was employed to assess the anti-inflammatory properties of AG and the compounds. Metabolomics was utilized to identify potential anti-inflammatory molecules in AG, while molecular dynamics simulations were conducted to forecast the interaction capabilities of these compounds with inflammatory targets. Additionally, macrophage cell was employed to investigate the anti-inflammatory mechanisms of the key molecules in AG by enzyme-linked immunosorbent assay and western blotting. Seven potential anti-inflammatory molecules were discovered in AG, with ginsenoside Rg1, ginsenoside Rs3 (G-Rs3), and oleanolic acid exhibiting the strongest affinity for signal transducer and activator of transcription 3. These compounds demonstrated inhibitory effects on macrophage migration in zebrafish models and the ability to regulate ROS levels in both zebrafish and macrophages. The cell experiments found that ginsenoside Rg1, ginsenoside Rs3, and oleanolic acid could promote macrophage M2/M1 polarization ratio and inhibit phosphorylation overexpression of signal transducer and activator of transcription 3. This study revealed the key anti-inflammatory molecules and mechanisms of AG, and provided new evidence of anti-inflammatory for the scientific use of AG.
研究领域:
药理学
·
免疫学
·
分子生物学
·
生物化学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULAR MEDICINE
·
2024
·Vol. 30
·期 1
·1-15
·
IF 6
Zhang FengQi,Zhang YiYang,Zhou JiaWang,Cai Ying,Li ZhiYu,Sun Jing,Xie ZhiJun,Hao GuiFeng
Background Rheumatoid arthritis, a chronic autoimmune disease, is characterized by synovial hyperplasia and cartilage erosion. Here, we investigated the potential mechanism of action of quercetin, the main component of flavonoids, in treating rheumatoid arthritis. Object To examine the anti-arthritic effects of quercetin and elucidate the specific mechanisms that differentiate its metabolic effects on autoimmune and inflammatory responses at the synovial cell level. Methods We created a collagen-induced arthritis (CIA) model in Wistar rats, which were administered quercetin (50 or 100 mg/kg) continuously for four weeks via stomach perfusion. The arthritis score, histopathological staining, radiological assessment, and serum biochemical parameters were used to study the impact of quercetin on disease improvement. Additionally, immunofluorescence was employed to detect JAK1/STAT3/HIF-1α expression in rat joints. Moreover, the effects of quercetin (20, 40, and 80 µmol/L) on the properties and behavior of synovial fibroblasts were evaluated in an in vitro MH7A cell model using flow cytometry, CCK8, and transwell assays. Further, the mRNA expression levels of inflammatory cytokines IL1β, IL6, IL17, and TNFα were assessed by quantitative real-time PCR. Glucose, lactate, lactate dehydrogenase, pyruvate, pyruvate dehydrogenase, and adenosine triphosphate assay kits were employed to measure the metabolic effects of quercetin on synovial fibroblasts. Finally, immunoblotting was used to examine the impact of quercetin on the JAK1/STAT3/HIF-1α signaling pathway in synovial fibroblasts. Results In vivo experiments confirmed the favorable effects of quercetin in CIA rats, including an improved arthritis score and reduced ankle bone destruction, in addition to a decrease in the pro-inflammatory cytokines IL-1β, IL-6, IL-17, and TNF-α in serum. Immunofluorescence verified that quercetin may ameliorate joint injury in rats with CIA by inhibiting JAK1/STAT3/HIF-1α signaling. Various in vitro experiments demonstrated that quercetin effectively inhibits IL-6-induced proliferation of MH7A cells and reduces their migratory and invasive behavior, while inducing apoptosis and reducing the expression of the pro-inflammatory cytokines IL1β, IL6, IL17, and TNFα at the mRNA level. Quercetin caused inhibition of glucose, lactate, lactate dehydrogenase, pyruvate, and adenosine triphosphate and increased pyruvate dehydrogenase expression in MH7A cells. It was further confirmed that quercetin may inhibit energy metabolism and inflammatory factor secretion in MH7A cells through JAK1/STAT3/HIF-1α signaling. Conclusions Quercetin’s action on multiple target molecules and pathways makes it a promising treatment for cartilage injury in rheumatoid arthritis. By reducing joint inflammation, improving joint metabolic homeostasis, and decreasing immune system activation energy, quercetin inhibits the JAK1/STAT3/HIF-1α signaling pathway to improve disease status.
研究领域:
免疫学
·
药理学
·
风湿病学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
CELL BIOLOGY INTERNATIONAL
·
2024
·
IF 3.3
Yuhua Zhang,Hanping Shi
This study explores the potential role and mechanism of Ginsenoside Rb3 (Rb3) in modulating osteoclastogenesis induced by human periodontal ligament fibroblasts (hPLFs) within the periodontitis microenvironment. We investigated the anti-inflammatory effects of Rb3 on hPLFs stimulated with Porphyromonas gingivalis lipopolysaccharide ( P.g -LPS) utilizing quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay techniques. Moreover, the functional role of Rb3 in hPLFs-induced osteoclast formation was assessed by treating human bone marrow-derived macrophages (hBMMs) with conditioned medium from hPLFs, followed by analyses through qPCR, western blot analysis, and staining for tartrate-resistant acid phosphatase (TRAP) and phalloidin. The impact of Rb3 on the activation of the STAT3 signaling pathway was determined via western blot analysis. Results indicated that Rb3 treatment significantly suppressed the upregulation of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1, and IL-18) at both gene and protein levels in hPLFs induced by P.g -LPS. Furthermore, conditioned medium from Rb3 plus P.g -LPS treated hPLFs notably decreased the number of TRAP-positive cells, actin ring formations, and the expression of osteoclast marker genes (including CTSK, NFATC1, and ACP5). Rb3 also inhibited the P.g -LPS-induced activation of the STAT3 pathway, with the activation of STAT3 partially reversing the effects of Rb3 on inflammation and osteoclast differentiation. Collectively, Rb3 ameliorates inflammation in P.g -LPS-stimulated hPLFs and reduces hPLFs-induced osteoclastogenesis by inhibiting the STAT3 signaling pathway, suggesting its potential as a therapeutic agent for periodontitis.
研究领域:
牙科学
·
药理学
·
免疫学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2025
·
IF 4.5
Xiaoqiang Huang,Guohua Ru,Hengyun Tian,Pengbo Zhang,Hongchang Zhao,Shouren Zhang,Sijie Wang,An Jia,Wanli Zhao
Background Benign prostatic hyperplasia (BPH) significantly compromises patients' quality of life, has detrimental effects on both physical and mental well-being, and poses a substantial economic burden. Current pharmacological interventions primarily focus on symptom relief; nevertheless, their associated adverse effects are evident. Rape bee pollen and maca are both homologous food products, which are not only rich in nutrition, but also have many biological activities. There is no report on the combination of rape bee pollen and maca in benign prostatic hyperplasia therapy, and no report on the molecular mechanism. This study aims to systematically investigate the therapeutic efficacy and underlying molecular mechanisms of a chewable tablet formulation containing rape bee pollen and maca in the management of BPH. Methods First, the chewable tablets were prepared from rape bee pollen and maca, and the High Performance Liquid Chromatography (HPLC) fingerprint was established. During a 4-week period, rats were subjected to subcutaneous injections of testosterone propionate solution to establish a BPH model, while simultaneously receiving orally administered chewable tablets for BPH treatment via gavage. We assessed the body weight, prostate tissue index, serum levels of dihydrotestosterone (DHT), testosterone (T), estradiol (E2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) levels in rats. Prostate tissues were collected for histopathological analysis. The protein expression levels of IL-6, phosphorylated Janus kinase 2 ( p -JAK2), and phosphorylated signal transducer and activator of transcription 3 ( p -STAT3) were determined by Western blotting. Rat feces were collected aseptically for 16S rDNA gene sequencing to assess gut microbiota levels. Additionally, our research findings demonstrate that the combined application of rape pollen and maca exhibits superior therapeutic efficacy compared to the individual use of either rape pollen or maca alone. Results We prepared the rape bee pollen and maca chewable tablets, established the HPLC fingerprint map, and quantitatively analyzed four of these main components. We found that the rape bee pollen and maca chewable tablets significantly inhibited DHT, T, E2, E2/T ratio, IL-6, TNF-α, and IL-1β and reduced MDA levels and increased SOD, GSH levels. 16S rDNA gene sequencing revealed that the chewable tablet increased the abundance of the beneficial bacteria Faecalibacterium, Collinsella, Phascolarctobacterium, Kineothrix , and Lactobacillus , and decreased that of the pro-inflammatory bacterium Prevotella . Western blot indicated that the chewable tablet could significantly inhibit the IL-6, p -JAK2, and p -STAT3 protein expression levels. Conclusion We found that rape bee pollen and maca chewable tablets had a protective effect on rats with BPH, and also found that the combination of rape bee pollen and maca was better than separate application. The mechanism may be related to the gut microbiota and IL-6/JAK2/STAT3 signaling pathway.
✓ 已验证
DOI
PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
·
2025
·
IF 2.5
Yingpei Miao,Shuqing Yu,Qingcui Zhang,Xiaomei Li,Bowei Xia,Li Yang,Xiaobin Li,Junwei He
Leonurus japonicus Houtt. (LJ) is a pivotal traditional Chinese medicine remedy for thrombosis; however, its potential mechanisms and active constituents remain unclear. In this study, LJ exhibits a significant antithrombotic effect on an arteriovenous bypass thrombosis rat, characterized by reductions in thrombus wet and dry weights, decreased maximum aggregation rate, increased thrombus formation inhibition rate, aggregation inhibition rate, alterations in fibrinogen and antithrombin III levels, and shortened coagulation indicators. Moreover, LJ significantly enhanced the erythrocyte staining area and intensity in an arachidonic acid-induced zebrafish heart. Network pharmacology indicated that LJ alleviates thrombosis by regulating TNF and IL-17 pathways. Metabolomics revealed that LJ significantly modulated 29 endogenous differential metabolites, linking it to the regulation of primary bile acid biosynthesis, IL-17, and TNF pathways. Zebrafish experiments and molecular docking suggested that kaempferol and apigenin exhibit antithrombotic effects by modulating TNF and IL-17 proteins. Finally, molecular dynamics simulation validated that kaempferol and apigenin have strong binding capabilities with TLR4, STAT3, TNF-α, and IL-17A, and their binding free energies are −20 to −27 and −13 to −15 kcal/mol, respectively. In conclusion, LJ exerts its antithrombotic effect by regulating lipid metabolism and inhibiting TLR4/STAT3/TNF-α/IL-17A pathways, with kaempferol and apigenin identified as bio-constituents. This plant holds significant potential for development and utilization in antithrombotic therapies. Graphical This study is the first to integrate network pharmacology, rat model, metabolomics, zebrafish model, molecular docking, and MD simulation techniques to elucidate the anti-thrombotic effect and mechanism of Leonurus japonicus by modulating lipid metabolism and inhibiting TLR4/STAT3/TNF-α/IL-17A pathways, with kaempferol and apigenin identified as primary pharmacological constituents.
研究领域:
药理学
·
中医药学
·
心血管疾病
·
系统生物学
·
计算生物学
·
动物学
·
生物信息学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2015
·
IF 3.574
Dongli Li,Zhiyun Du,Chenyue Li,Yue Liu,Susan Goodin,Huarong Huang,Yan He,Yuan Zhang,Huaqian Wang,Xi Zheng,Kun Zhang
Five terpenoids ( 1 – 5 ) from a vegetable plant Acanthopanax trifoliatus (L.) Merr. were investigated for their effects on human prostate cancer cells. The diterpenoid ( 3 ) and triterpenoids ( 4 and 5 ) were found to inhibit the growth and stimulate apoptosis in PC-3 cells. The effects of these terpenoids on PC-3 cells were associated with strong suppression of nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3). These terpenoids also inhibited the expression of survivin, a downstream target of NF-κB and STAT3. The in vivo study using a xenograft mouse model showed that 5 strongly inhibited the formation and growth of PC-3 tumours. Moreover, treatment with 5 strongly decreased the expression of phospho-STAT3 and survivin in PC-3 tumours. Our results indicate that 5 has preventive efficacy on the development of PC-3 xenograft tumours. This terpenoid may serve as a candidate for future development as a novel agent for prostate cancer prevention.
研究领域:
肿瘤学
·
药理学
·
分子生物学
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）