ACTA HISTOCHEMICA
·
2024
·
IF 2.3
Ni Tang,Yunhui Li,Junchi Tang,Juexin Chen,Lili Chen,Lin Dang
Cutaneous melanoma (cM) is a prevalent invasive cancer resulting from the malignant transformation of melanocytes. At present, the primary treatment for melanoma is surgical resection, which is not appropriate for patients with metastasis. Therefore, it is necessary to identify effective therapeutic targets for the early diagnosis and treatment of metastatic melanoma. Acyl-CoA thioesterase 7 (ACOT7) has been reported to be involved in the progression of multiple cancer, while its role in melanoma has not been extensively researched. Through gain-of-function and loss-of-function experiments, ACOT7 was identified as a tumor promoter that facilitates the progression of melanoma cells. Cell proliferation was promoted by overexpressing ACOT7 in M14 cells, and was suppressed by silencing ACOT7 in MeWo cells. Knockdown of ACOT7 induced cell cycle arrest by increasing the expressions of cyclin dependent kinase inhibitor 1B (P27) and cyclin dependent kinase inhibitor 1 A (P21), while simultaneously reducing proliferating cell nuclear antigen (PCNA) expression. Upregulation of ACOT7 promoted the cell cycle of melanoma cells. Additionally, apoptosis was induced by the absence of ACOT7 through activating caspase-3 and poly (ADP-ribose) polymerase (PARP). The metastatic and invasive capacity of melanoma cells was significantly enhanced by the overexpression of ACOT7 and inhibited by the downregulation of ACOT7. Moreover, the cAMP responsive element binding protein 1 (CREB1) positively regulates ACOT7 expression by binding to its promoter region. A decrease of cell proliferation, migration and invasion, as well as an increase of cell apoptosis induced by silencing CREB1 were obviously reversed by ACOT7. In summary, ACOT7 transcriptionally activated by CREB1 elevates the progression of cM.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
CELLULAR SIGNALLING
·
2024
·
IF 4.4
Zheng-Ming Cao,Su Fu,Chao Dong,Teng-Yue Yang,Xiao-Kang Liu,Chun-Lin Zhang,Dong-Zhe Li
The progression of osteoarthritis (OA) includes the initial inflammation, subsequent degradation of the extracellular matrix (ECM), and chondrocyte apoptosis. Down syndrome candidate region 1 (DSCR1) is a stress-responsive gene and expresses in varied types of cells, including chondrocytes. Bioinformatics analysis of GSE103416 and GSE104739 datasets showed higher DSCR1 expression in the inflamed cartilage tissues and chondrocytes of OA. DSCR1 had two major isoforms, isoform 1 (DSCR1–1) and isoform 4 (DSCR1–4). We found that DSCR1–1 had a faster ( in vitro ) and higher expression ( in vivo ) response to OA compared to DSCR1–4. IL-1β-induced apoptosis, inflammation, and ECM degradation in chondrocytes were attenuated by DSCR1–1 overexpression. DSCR1–1 triggered the phosphorylation of cAMP response element-binding 1 (CREB1) at 133 serine sites by decreasing calcineurin activity. Moreover, activated CREB1 moved into the cell nucleus and combined in the promoter regions of aldehyde dehydrogenase 2 (ALDH2), thus enhancing its gene transcription. ALDH2 could recover Wnt/β-catenin signaling transduction by enhancing phosphorylation of β-catenin at 33/37 serine sites and inhibiting the migration of β-catenin protein from the cellular matrix to the nucleus. In vivo , adenoviruses (1 × 10 8 PFU) overexpressing DSCR1–1 were injected into the articular cavity of C57BL/6 mice with medial meniscus surgery-induced OA, and it showed that DSCR1–1 overexpression ameliorated cartilage injury. Collectively, our study demonstrates that DSCR1–1 may be a potential therapeutic target of OA.
研究领域:
骨科
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2021
·
IF 4.219
Lei Yu,Xiuguo Gan,Yufeng Bai,Ruihua An
Kidney stone disease (KSD) is a common urinary disease with increasing prevalence worldwide. In this study, we investigated the effect of cyclic AMP responsive element binding protein (CREB) 1 in a KSD model of rat and calcium oxalate monohydrate (COM) crystals-treated NRK-52E cells. Rats were pretreated with lentivirus (LV)-CREB1 vector or LV-control vector and administrated with ethylene glycol + ammonium chloride to induce KSD. It was found that CREB1 was activated in the renal tissue of non-treated KSD rats. Pretreating with LV-CREB1 vector significantly enhanced CREB1 expression in KSD rats. Biochemical analysis for serum and urine showed that upregulation of CREB1 could improve the renal function of KSD rats. Histological analysis confirmed that upregulation of CREB1 alleviated the renal injury in KSD rats. Moreover, the upregulation of CREB1 suppressed the apoptosis in renal tissue of KSD rats through regulating apoptosis-associated proteins. Further study showed that the upregulation of CREB1 could attenuate the oxidative stress in KSD rats as well. More interestingly, the upregulation of CREB1 enhanced the activity of complex I and complex III and the expression of mitochondrial cytochrome c , implicating the effect of CREB1 on improving mitochondrial function in KSD rats. In vitro study confirmed that upregulation of CREB1 inhibited the apoptosis and oxidative stress, while improved the mitochondrial function of NRK-52E cells treated with COM crystals, demonstrating the protective effect of CREB1 on COM crystals-induced renal epithelial cell injury. Therefore, CREB1 might be served as a promising target in the prophylaxis and treatment of KSD.
研究领域:
肾病学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2026
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IF 6.6
Yan Bai,Ji Feng,Xiao-Yu Wu,Zhi-Sheng Yao,Yue-Tong Liu,Yu-Hong Li,Guo-Dong Lu,Kun Xue
Background Aspartame, a widely used non-nutritive sweetener, has been associated with potential neurotoxicity. However, it remains unclear whether aspartame consumption can exacerbate cerebral ischemia–reperfusion injury (CIRI), a major contributor to stroke outcomes, and the underlying mechanisms are poorly understood. Methods In vivo , male C57BL/6 J mice were given free access to 0.1% or 0.2% (w/v, equivalent to human acceptable daily intake level) aspartame, for 7 days, followed by bilateral common carotid artery occlusion (BCCAO) to induce CIRI. In vitro , hippocampal neural stem cells (NSCs) were subjected to oxygen–glucose deprivation (OGD) with aspartame. Cell injury, general and mitochondrial reactive oxygen species (ROS) burden, and mitochondrial function were assessed. Gene Ontology (GO), KEGG enrichment, and protein–protein interaction (PPI) network analyses were performed to identify potential targets. The ERK/CREB1 signaling pathway was evaluated by western blotting and pharmacological modulation. Results Aspartame significantly increased the infarct volume and aggravated neuronal damage in BCCAO-treated mice. In NSCs, aspartame, but not acesulfame or sucralose, selectively enhanced OGD-induced apoptosis, accompanied by mitochondrial depolarization and excessive ROS accumulation, while showing minimal effects under normoxia conditions. GO/KEGG and PPI analyses highlighted ERK/CREB1 as an important node in aspartame-induced neurotoxicity. Consistently, aspartame suppressed the phosphorylation of ERK1/2 and CREB1. The ERK activator LM22B-10 and mitochondria-targeted antioxidant Mito-TEMPO partially reversed mitochondrial dysfunction, apoptosis and ERK/CREB1 suppression. Additionally, aspartame increased the mRNA expression of pro-inflammatory cytokines (TNF- α , IL-1 β and IL-6) and increased NF-κB p65 phosphorylation and reduced the proportion of Tuj1-positive cells, which were mitigated by ERK activation. Conclusion Aspartame exacerbates CIRI-associated injury in a stress-dependent manner, involving mitochondrial dysfunction, ROS accumulation, and ERK/CREB1 suppression. Future studies are warranted to explore the long-term neurobehavioral outcomes and validate these mechanisms in clinical scenarios.
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高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2026
·Vol. 27
·期 16
·7218
·
IF 5.6
Li Xie,Shanliang Yuan,Lu Gan,Rongheng Ma,Lei Tang,Qiang Xu,Weihong Li
Bisphenols (BPs) are widespread environmental endocrine disruptors, but their potential depression-related neurotoxicity has not been systematically assessed. Here, we combined machine learning (ML), network toxicology, molecular docking, and in vivo experiments to screen 26 bisphenols for depression-related neurotoxic risk. We first integrated bisphenol A (BPA)-related targets with depression-related genes to build a chemical-gene-phenotype-disease network and an adverse outcome pathway (AOP) framework. We then used nine ML algorithms to rank the predicted risk of the 26 bisphenols. Molecular docking showed that the predicted high-risk compounds had strong binding affinity for estrogen receptor 1 (ESR1). The AOP analysis further suggested the involvement of the ESR1–cAMP response element-binding protein 1 (CREB1)–glutamate ionotropic receptor N-methyl-D-aspartate type subunit 2B (GRIN2B) pathway. In vivo experiments showed that BPA exposure caused neuronal damage in the cornu ammonis 3 (CA3) region of the rat hippocampus and significantly reduced the messenger RNA (mRNA) expression of the corresponding genesEsr1,Creb1, andGrin2bin hippocampal tissue. Overall, this study screened and prioritized the model-predicted depression-related neurotoxic risk of 26 bisphenols, supports a role for the ESR1–CREB1–GRIN2B pathway in BPA-induced neurotoxicity, and provides mechanistic evidence for bisphenol risk assessment.
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高影响因子
MOLECULAR IMMUNOLOGY
·
2026
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IF 3.7
Suhong Ye,Ling Bao,Qiaolu Xu,Zihan Ding,Fei Wu,Xia Yuan,Yang Zhou,Nashwa Amin,Javaria Sundus,Marong Fang
Dihydroartemisinin (DHA) dose-dependently ameliorates ischemic brain injury and promotes neurological recovery in mice after ischemic stroke. • DHA inhibits ferroptosis in ischemic brain tissue via regulating iron homeostasis, lipid peroxidation and core ferroptosis-related proteins. • Astrocytic TAK1-CREB1 signaling pathway is identified as the key molecular target mediating the neuroprotective effects of DHA. • This study provides a promising drug repurposing candidate and novel therapeutic target for the clinical treatment of ischemic stroke. Background Ischemic stroke accounts for 87% of all stroke cases, and remains a leading cause of mortality and disability worldwide. Current reperfusion therapies are limited by narrow therapeutic windows, and cerebral ischemia-reperfusion injury (CIRI) remains a major clinical challenge. Ferroptosis, an iron-dependent form of regulated cell death characterized by lethal lipid peroxidation, has been identified as a key pathological driver of CIRI. Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, has shown neuroprotective effects in ischemic stroke, but its underlying mechanism, especially the regulatory effect on ferroptosis via the TAK1-CREB1 signaling axis, remains unclear. Objective To investigate the neuroprotective effect of DHA in ischemic stroke and its molecular mechanism related to the TAK1-CREB1 signaling pathway and ferroptosis regulation. Methods Wild-type (WT) C57BL/6 J mice and astrocyte-specific CREB1 conditional knockout (CREB1 CKO) mice were used to establish a photothrombotic stroke (PTs) model. Neurological function was evaluated by modified neurological severity score (mNSS), Bederson score, Garcia scale and hanging test. Cerebral infarct volume was measured by TTC staining. Cerebral blood flow (CBF) was detected by laser speckle contrast imaging. Histopathological changes were observed by HE and Nissl staining. Mitochondrial ultrastructure was examined by transmission electron microscopy (TEM). The levels of malondialdehyde (MDA), glutathione (GSH), NADPH/NADP + ratio, ferrous iron (Fe 2+ ) and total iron in brain tissue were detected by biochemical kits. The expression of ferroptosis-related proteins and CREB1 was detected by Western blot and immunofluorescence staining. Results DHA treatment dose-dependently improved neurological function, reduced infarct volume, restored CBF, and ameliorated histopathological damage in PTs mice. TEM revealed that DHA reversed ferroptosis-typical mitochondrial changes in ischemic brain tissue. Biochemically, DHA decreased MDA, Fe²⁺, and total iron, while increasing GSH and NADPH/NADP⁺ ratio. Mechanistically, DHA dose-dependently upregulated GPX4, xCT, and FTH1, and downregulated ACSL4. Notably, astrocyte-specific CREB1 knockout nearly completely abolished DHA's neuroprotective and anti-ferroptosis effects. Conclusion DHA promotes neurological rehabilitation after ischemic stroke by targeting the astrocytic TAK1-CREB1 signaling pathway to inhibit ferroptosis. This study provides a novel theoretical basis and promising candidate drug for the clinical treatment of ischemic stroke.
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PubMed
高影响因子
BRITISH JOURNAL OF CANCER
·
2025
·
IF 6.8
Chen Xiao,Cao Lixia,Feng Mengdan,Shuai Qiuying,Guo Min,Li Zhaoxian,Qi Chunchun,Shi Jie,Liu Yuxin,Zuo Siyu,Yu Tianwen,Hu Huayu,Wang Yanjing,Xue Yao,Sun Peiqing,Shi Yi,Wang Hang,Liu Lei,Yang Shuang
Background Breast cancer cells that break through the basement membrane interact directly with neighboring adipocytes. Therefore, adipocytes adjacent to the invasive front of tumour undergo lipolysis and transform into cancer-associated adipocytes (CAAs), which is vital for the malignant progression of breast cancer. However, tumor-derived factors that trigger this process are still to be determined. Methods Transcriptome sequencing was used to identify the downstream transcription factor of adrenomedullin (AM). Tet-On system was used to construct the 3T3-L1 cell line with inducible overexpression of Zeb1. Adipocyte-specific knock-in Zeb1 transgenic mice ( Zeb1 adiTG ) were used to construct an allograft tumor model. Results Breast cancer cell-derived AM downregulated the transcriptional expression of Zeb1 by triggering the cAMP/PKA/Creb1 pathway, thereby exerting lipolytic effects in CAAs. On the contrary, adipose tissue-specific upregulation of Zeb1 significantly attenuated AM-induced lipolytic phenotypes. Of note, we used the Zeb1 adiTG mice to construct allograft tumor models. The results confirmed that breast cancer cell-derived AM conferred tumorigenicity in vivo, which effect was predominantly dependent on the aberrant expression of adipocyte-specific Zeb1. Conclusions These findings collectively suggested that breast cancer cell-derived AM promotes lipid metabolic reprogramming through a Zeb1-dependent manner in CAAs, which displays significant clinical implications and may provide promising therapeutic approaches for targeting the breast cancer-associated adipose microenvironment.
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高影响因子
JOURNAL OF PHARMACY AND PHARMACOLOGY
·
2025
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IF 3.2
Yao Wang,Hua Dong-Ming,Wang Wen-kai,Zhang Zhao-zhou,Guan Yun-Feng,Wang Yan
ObjectiveTo investigate the mechanism of ginsenoside Rb1 (G-Rb1) against colorectal cancer under chronic stress.MethodsA chronic restraint stress (CRS) model and a colorectal cancer (CRC) subcutaneous xenograft model were established. Western blot analysis quantified β2-adrenergic receptor (β2-AR), cAMP response element-binding protein 1 (CREB1), and p-CREB1 expression. Additionally, glycolytic enzymes GLUT1, HK2, and PFKP were analyzed via Western blot and RT-qPCR, with glucose uptake, lactate, ATP, and stress hormone levels assessed by flow cytometry, kits, and ELISA.Key findingsCompared to the control group, the stress group exhibited increased tumor volume and mass, along with elevated expression of β2-AR, p-CREB1, and upregulated expression levels of GLUT1, HK2, and PFKP. Additionally, glucose, lactate, and epinephrine levels were higher in the stress group. In comparison to the stress group, G-Rb1 treatment demonstrated reduced tumor volume and mass, decreased p-CREB1 expression, as well as downregulated protein and mRNA levels of GLUT1, HK2, and PFKP. Glucose, lactate, and epinephrine levels also showed a reduction in the G-Rb1-treated groups.ConclusionsG-Rb1 suppresses the growth of colorectal cancer under chronic stress, potentially through downregulation of the β2-AR/CREB1 signaling pathway, thereby reducing glycolytic activity in colorectal cancer under chronic stress.
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PubMed
高影响因子
Translational Cancer Research
·
2026
·Vol. 15
·期 2
·97
·
IF 2.1
Xiang Lei,Shi Jinjie,Huang Xueqing,Zhou Shi
Background Donafenib (DON) has been found to be effective in prolonging progression-free survival for advanced hepatocellular carcinoma (HCC), although it remains limited in improving long-term survival outcomes. Quercetin (QUE) has also been demonstrated to exhibit anticancer effects in various malignant tumors. The most recent research has shown that the combination therapy of QUE and conventional chemotherapy drugs can enhance its anti-cancer activity. Therefore, this study aimed to investigate whether QUE and DON in combination could synergistically suppress tumor growth in HepG2 cells. Methods In this study, the effects of QUE alone and in combination with DON were assessed on HCC HepG2 cells. Both in vitro and in vivo (subcutaneous xenograft models in nude mice) experiments were conducted. The expression of cyclic AMP-responsive element-binding protein 1 (CREB1), a putative common target, was evaluated, and its role in lipid metabolism was investigated. Results CREB1 was confirmed to be highly expressed in HepG2 cells and serves as a molecular target for both QUE and DON. Suppressing CREB1 expression significantly inhibited lipid metabolism and reduced the biological activity of HepG2 cells. Furthermore, QUE, both alone and in combination with DON, was shown to down-regulate the CREB1/dynamin-related protein 1 (DRP1)/sterol regulatory element-binding protein 1 (SREBP1) signaling axis. This inhibition significantly suppressed lipid metabolism and tumor growth in the nude mouse xenograft models. Conclusions These findings indicate that the combination of QUE and DON exerts its antitumor effects by inhibiting the CREB1/DRP1/SREBP1 axis mediated lipid metabolism pathway in HepG2 cells. This offers a novel potential approach for enhancing the therapeutic efficacy of DON in the treatment of HCC.
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高影响因子
Cancer Communications
·
2023
·Vol. 43
·期 3
·338-364
·
IF 16.2
Peng Xia,Hao Zhang,Haofeng Lu,Kequan Xu,Xiang Jiang,Yuke Jiang,Xiangdong Gongye,Zhang Chen,Jie Liu,Xi Chen,Weijie Ma,Zhonglin Zhang,Yufeng Yuan
Background Hepatocellular carcinoma (HCC) is one of the most prevalent cancers in the world, with a high likelihood of metastasis and a dismal prognosis. The reprogramming of glucose metabolism is critical in the development of HCC. The Warburg effect has recently been confirmed to occur in a variety of cancers, including HCC. However, little is known about the molecular biological mechanisms underlying the Warburg effect in HCC cells. In this study, we sought to better understand how methyltransferase 5, N6-adenosine (METTL5) controls the development of HCC and the Warburg effect. Methods In the current study, quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of METTL5 in HCC tissues and cell lines. Several different cell models and animal models were established to determine the role of METTL5 in glucose metabolism reprogramming and the underlying molecular mechanism of HCC. Glutathione-S-transferase pulldown, coimmunoprecipitation, RNA sequencing, non-targeted metabolomics, polysome profiling, and luciferase reporter assays were performed to investigate the molecular mechanisms of METTL5 in HCC cells. Results We discovered that METTL5 drove glucose metabolic reprogramming to promote the proliferation and metastasis of HCC. Mechanistically, upregulation of METTL5 promoted c-Myc stability and thus activated its downstream glycolytic genes lactate dehydrogenase A ( LDHA ), enolase 1 ( ENO1 ), triosephosphate isomerase 1 ( TPI1 ), solute carrier family 2 member 1 ( SLC2A1 ), and pyruvate kinase M2 ( PKM2 ). The c-Box and ubiquitin binding domain (UBA) regions of ubiquitin specific peptidase 5 (USP5) binded to c-Myc protein and inhibited K48-linked polyubiquitination of c-Myc. Further study revealed that METTL5 controled the USP5 translation process, which in turn regulated the ubiquitination of c-Myc. Furthermore, we identified cAMP responsive element binding protein 1 (CREB1)/P300 as a critical transcriptional regulator of METTL5 that promoted the transcription of METTL5 in HCC. In patient-derived tumor xenograft (PDX) models, adenovirus-mediated knockout of METTL5 had a good antitumor effect and prolonged the survival of PDX-bearing mice. Conclusions These findings point to a novel mechanism by which CREB1/P300-METTL5-USP5-c-Myc controls abnormal glucose metabolism and promotes tumor growth, suggesting that METTL5 is a potential therapeutic target and prognostic biomarker for HCC.
研究领域:
癌症生物学
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分子生物学
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细胞生物学
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生物化学
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转化医学
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PubMed
高影响因子
RESEARCH IN VETERINARY SCIENCE
·
2023
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IF 2.4
Dongliu Luo,Yiming Lu,Qiaohan Liu,Hang Yin,Xiaodan Huang,Shu Li
Cadmium (Cd) is toxic non-essential heavy metal that precipitates adverse health effects in humans and animals, but the effect of Cd on lymph node toxicity of piglets is still unclear. In order to explore the possible molecular mechanism of Cd toxicity to lymph nodes of piglets, ten 6-week-old male weaned piglets were randomly divided into two groups, C group and Cd group. Group C was fed with basal diet, while group Cd was fed with basal diet supplemented with CdCl 2 (20 mg/kg) for 40 days, the pigs were euthanized and the mesenteric, inguinal and submandibular lymph nodes (MLN, ILN, SLN) were collected. The results indicated that Cd could induce the inflammatory cell infiltration , microvascular hemorrhage, microthrombosis and cell necrosis in MLN, ILN and SLN of piglets, induced Cytochrome P450 proteins (CYP1A1、CYP2E1、CYP2A1 and CYP3A2) mRNA levels and the protein levels of Vitamin D receptor (VDR) and cAMP response element binding protein 1 (CREB1). In addition, Cd exposure upregulated the mRNA and protein levels of dynamin-related protein 1 (DRP1), receptor-interacting protein kinase 3 (RIP3), mixed lineage kinase domain-like protein (MLKL), and increased tumor necrosis factor-α (TNFα), interferon-γ (IFNγ), interleukin-2 (IL-2), interleukin-4 (IL-4), cyclooxygenase 2 (COX-2) protein levels, and the damage degree of three kinds of lymph nodes was similar after Cd exposure. In general, these results manifest that Cd exposure regulates VDR/CREB1 pathway, activates CYP450s , induces necroptosis of lymph nodes, and leads to inflammation.
研究领域:
毒理学
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免疫学
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分子生物学
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动物科学
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PubMed
高影响因子
Bioengineered
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2021
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IF 3.269
Jing Wang,Yan Liu,Hongbing Cai,Hong Jiang,Wei Li,Yuying Shi
Cervical cancer (CC) is one of the most common malignancies among women. It has been demonstrated that long coding RNAs (lncRNAs) play a crucial role in CC. The purpose of this study was to investigate the role of the colon cancer associated transcript 2 (CCAT2) lncRNA in CC and elucidate its possible mechanisms of action. The expression of CCAT2, the miR-493-5p microRNA (miRNA), and mRNA was detected using qRT-PCR. Cell viability, proliferation, and migration and invasion were determined using the MTT, colony formation, and transwell assays, respectively. The interactions between miR-493-5p and CCAT2 or cAMP response element-binding protein 1 (CREB1) were verified using the luciferase and RNA pull-down assays. The effects of CCAT2 knockdown on in vivo tumor growth were determined using tumor xenografts and immunohistochemistry assays. The expression of CCAT2 was upregulated in CC cells and tissues. However, the knockdown of CCAT2 inhibited the proliferation and epithelial-mesenchymal transition (EMT) of CC cells in vitro and suppressed tumor growth in vivo. Mechanistically, CCAT2 functions as a competing endogenous RNA (ceRNA) to upregulate the expression of CREB1 by binding to miR-493-5p. The overexpression of CREB1 or downregulation of miR-493-5p antagonized the effect of CCAT2 knockdown on the proliferation and EMT of CC cells. The knockdown of CCAT2 suppressed the aggressiveness of CC via the miR-493-5p/CREB1 axis. Therefore, CCAT2 is likely to be a promising therapeutic target for CC.
研究领域:
肿瘤学
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分子生物学
·
细胞生物学
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DOI
PubMed
高影响因子
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