共查询到20条相似文献,搜索用时 15 毫秒
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Wenzhe Yin Jun Xu Chao Li Xiankui Dai Tong Wu Jifeng Wen 《Cell biology international》2020,44(8):1616-1627
As a potential antitumor herbal medicine, plantamajoside (PMS) benefits the treatment of many human malignances. However, the role of PMS in the progression of hepatocellular carcinoma (HCC) and the related molecular mechanisms is still unknown. Here, we proved that the cell viabilities of HepG2 cells were gradually decreased with the increasing concentrations of CoCl2 and/or PMS via cell counting kit‐8 assay. Meanwhile, 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) and western blot assays were used to further confirm that PMS inhibited the CoCl2‐induced cell proliferation in HepG2 cells via suppressing the Ki67 and proliferating cell nuclear antigen expressions. We also performed wound‐healing and transwell assays and demonstrated that PMS inhibited CoCl2‐induced migration and invasion in HepG2 cells via suppressing the epithelial–mesenchymal transition (EMT) process. In addition, the use of 3‐(5′‐hydroxymethyl‐2′‐furyl)‐1‐benzylindazole further proved that PMS inhibited the malignant biological behaviors of HepG2 cells under hypoxic condition by suppressing the hypoxia‐inducible factor‐1α (HIF‐1α) expression. Besides, we further confirmed that PMS suppressed the growth and metastasis of implanted tumors in vivo. Given that PMS suppressed the proliferation and EMT induced by CoCl2 in HCC cells via downregulating HIF‐1α signaling pathway, we provided evidence that PMS might be a novel anti‐cancer drug for HCC treatment. 相似文献
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Xiaohua Li Xue Li Shikun He Mingwei Zhao 《Journal of cellular and molecular medicine》2020,24(16):9420-9427
Proliferative vitreoretinopathy (PVR) is a blinding eye disease. Epithelial‐mesenchymal transition (EMT) of RPE cells plays an important role in the pathogenesis of PVR. In the current study, we sought to investigate the role of the methyl‐CpG‐binding protein 2 (MeCP2), especially P‐MeCP2‐421 in the pathogenesis of PVR. The expressions of P‐MeCP2‐421, P‐MeCP2‐80, PPAR‐γ and the double labelling of P‐MeCP2‐421 with α‐SMA, cytokeratin, TGF‐β and PPAR‐γ in human PVR membranes were analysed by immunohistochemistry. The effect of knocking down MeCP2 using siRNA on the expressions of α‐SMA, phospho‐Smad2/3, collagen I, fibronectin and PPAR‐γ; the expression of α‐SMA stimulated by recombinant MeCP2 in ARPE‐19; and the effect of TGF‐β and 5‐AZA treatment on PPAR‐γ expression were analysed by Western blot. Chromatin immunoprecipitation was used to determine the binding of MeCP2 to TGF‐β. Our results showed that P‐MeCP2‐421 was highly expressed in PVR membranes and was double labelled with α‐SMA, cytokeratin and TGF‐β, knocking down MeCP2 inhibited the activation of Smad2/3 and the expression of collagen I and fibronectin induced by TGF‐β. TGF‐β inhibited the expression of PPAR‐γ, silence of MeCP2 by siRNA or using MeCP2 inhibitor (5‐AZA) increased the expression of PPAR‐γ. α‐SMA was up‐regulated by the treatment of recombinant MeCP2. Importantly, we found that MeCP2 bound to TGF‐β as demonstrated by Chip assay. The results suggest that MeCP2 especially P‐MeCP2‐421 may play a significant role in the pathogenesis of PVR and targeting MeCP2 may be a potential therapeutic approach for the treatment of PVR. 相似文献
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Yanfen Zou Shuhong Li Dan Wu Yetao Xu Sailan Wang Ying Jiang Fang Liu Ziyan Jiang Hongmei Qu Xiang Yu Xiaoli Wang Yuanli Wang Lizhou Sun 《Journal of cellular and molecular medicine》2019,23(4):2702-2710
Impairment spiral arteries remodelling was considered to be the underlying cause of pathogenesis of pre‐eclampsia (PE). Resveratrol (RE) was reported that it could modulate cellar phenotype to ameliorate diverse human diseases. However, the biological function of RE in PE remains poorly understood. In this report, we investigated the effect of RE on trophoblast phenotype both in vivo and in vitro. We conducted MTT and transwell assays to explore cell proliferation and invasion events in HTR‐8/SVneo. In mice model, the clinical characteristics of PE were established through the injection of NG‐nitro‐l ‐arginine methyl ester (L‐NAME). Furthermore, related experiments were performed to detect cellar phenotype‐associated signalling pathway, including epithelial‐mesenchymal transition (EMT) and Wnt/β‐catenin. Cell assays indicated that RE could increase trophoblasts migration and invasion. In addition, hypertension and proteinuria were markedly ameliorated by RE compared with the controls in PE mice model. Moreover, treatment by RE in trophoblasts or in PE model, we found that RE activated EMT progress through the regulation of E‐cadherin, β‐catenin, N‐cadherin, vimentin expression, and further altered the WNT‐related gene expression, including WNT1, WNT3 and WNT5B. Our findings demonstrated that RE might stimulate the invasive capability of human trophoblasts by promoting EMT and mediating the Wnt/β‐catenin pathway in PE. 相似文献
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MiR‐30c protects diabetic nephropathy by suppressing epithelial‐to‐mesenchymal transition in db/db mice 下载免费PDF全文
Yanru Zhao Zhongwei Yin Huaping Li Jiahui Fan Shenglan Yang Chen Chen Dao Wen Wang 《Aging cell》2017,16(2):387-400
Epithelial‐to‐mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR‐30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the roles of miR‐30c in EMT and tubulointerstitial fibrosis, recombinant adeno‐associated viral vector was applied to manipulate the expression of miR‐30c. In vivo study showed that overexpression of miR‐30c suppressed EMT, attenuated renal tubulointerstitial fibrosis and reduced proteinuria, serum creatinine, and BUN levels. In addition, Snail1 was identified as a direct target of miR‐30c by Ago2 co‐immunoprecipitation, luciferase reporter, and Western blot assays. Downregulating Snail1 by siRNA reduced high glucose‐induced EMT in HK2 cells, and miR‐30c mimicked the effects. Moreover, miR‐30c inhibited Snail1‐TGF‐β1 axis in tubular epithelial cells undergoing EMT and thereby impeded the release of TGF‐β1; oppositely, knockdown of miR‐30c enhanced the secretion of TGF‐β1 from epitheliums and significantly promoted proliferation of fibroblasts and fibrogenesis of myofibroblasts, aggravated tubulointerstitial fibrosis, and dysfunction of diabetic nephropathy. These results suggest a protective role of miR‐30c against diabetic nephropathy by suppressing EMT via inhibiting Snail1‐TGF‐β1 pathway. 相似文献
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HIF‐2α activated lncRNA NEAT1 promotes hepatocellular carcinoma cell invasion and metastasis by affecting the epithelial‐mesenchymal transition 下载免费PDF全文
Xiaowei Zheng Yiwen Zhang Yujia Liu Luo Fang Li Li Jiao Sun Zongfu Pan Wenxiu Xin Ping Huang 《Journal of cellular biochemistry》2018,119(4):3247-3256
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Lu Ge Huizhi Wang Xiao Xu Zhengrong Zhou Junbo He Wanxin Peng Fengyi Du Youli Zhang Aihua Gong Min Xu 《Journal of cellular and molecular medicine》2020,24(2):1969-1979
Protein arginine methyltransferase 5 (PRMT5) has been implicated in the development and progression of human cancers. However, few studies reveal its role in epithelial‐mesenchymal transition (EMT) of pancreatic cancer cells. In this study, we find that PRMT5 is up‐regulated in pancreatic cancer, and promotes proliferation, migration and invasion in pancreatic cancer cells, and promotes tumorigenesis. Silencing PRMT5 induces epithelial marker E‐cadherin expression and down‐regulates expression of mesenchymal markers including Vimentin, collagen I and β‐catenin in PaTu8988 and SW1990 cells, whereas ectopic PRMT5 re‐expression partially reverses these changes, indicating that PRMT5 promotes EMT in pancreatic cancer. More importantly, we find that PRMT5 knockdown decreases the phosphorylation level of EGFR at Y1068 and Y1172 and its downstream p‐AKT and p‐GSK3β, and then results in down‐regulation of β‐catenin. Expectedly, ectopic PRMT5 re‐expression also reverses the above changes. It is suggested that PRMT5 promotes EMT probably via EGFR/AKT/β‐catenin pathway. Taken together, our study demonstrates that PRMT5 plays oncogenic roles in the growth of pancreatic cancer cell and provides a potential candidate for pancreatic cancer treatment. 相似文献
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IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway 下载免费PDF全文
Jian Zhou Shutao Zheng Tao Liu Qing Liu Yumei Chen Doudou Tan Rong Ma Xiaomei Lu 《Journal of cellular biochemistry》2018,119(8):7040-7052
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miR‐96 regulates migration and invasion of bladder cancer through epithelial‐mesenchymal transition in response to transforming growth factor‐β1 下载免费PDF全文
Chunfeng He Qingchuan Zhang Renze Gu Yujiao Lou Wei Liu 《Journal of cellular biochemistry》2018,119(9):7807-7817
Bladder cancer (BC) is one of the most frequent urological malignancies, and its molecular mechanism still remains unclear. Recent studies have revealed that MicroRNA (miRNAs) acted as oncogenes or tumor suppressors in a variety of cancers. MiRNA‐96 has been reported to play a significant role in the development and progression of many cancers. In the current study, we found that transforming growth factor (TGF)‐β1 played a significant role in the progression that miR‐96 conducted. And TGF‐β1 could also regulate the expression of FOXQ1, which is the target gene of miR‐96. Furthermore, miR‐96 induced epithelial‐mesenchymal transition in BC cells, which is driven by TGF‐β1. In conclusion, our data revealed that miR‐96 regulates the progression and epithelial‐mesenchymal transition, which is driven by TGF‐β1 in BC cells; it may provide a new thought for the therapy of BC. 相似文献
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Xin He Nana Liu Tianyi Mu Dan Lu Chanwei Jia Shuyu Wang Chenghong Yin Lingyan Liu Liying Zhou Xiaowu Huang Yanmin Ma 《Journal of cellular and molecular medicine》2020,24(17):9658-9666
Endometriosis is a common, chronic gynaecologic disease affecting up to 10% of women in their reproductive age and leading to pain and infertility. Oestrogen (E2)‐induced epithelial‐mesenchymal transition (EMT) process has been considered as a key factor of endometriosis development. Recently, the dysregulated circular RNAs (circRNAs) have been discovered in endometriosis tissues. However, the molecular mechanism of circRNAs on the E2‐induced EMT process in endometriosis is still unknown. Here, we demonstrated that circ_0004712 up‐regulated by E2 treatment in endometrial epithelial cells. Knock‐down the expression of circ_0004712 significantly suppressed E2‐induced cell migration activity. Meanwhile, we identified miR‐148a‐3p as a potential target miRNA of circ_0004712. Inhibited the expression of miR‐148a‐3p could recovered the effect of circ_0004712 knock‐down in E2‐treated endometrial epithelial. Furthermore, Western blot assay showed that E2 treatment could increase the expression and activity of β‐catenin, snail and N‐cadherin and reduce the expression of E‐cadherin. The expression and activity of β‐catenin pathway were recovered by circ_0004712 knock‐down or miR‐148a‐3p overexpression. Altogether, the results demonstrate that circ_0004712/miR‐148a‐3p plays an important role in E2‐induced EMT process in the development of endometriosis, and the molecular mechanism may be associated with the β‐catenin pathway. This work highlighted the importance of circRNAs in the development of endometriosis and provide a new biomarker for diagnosis and therapies. 相似文献
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Tumor‐suppressive roles of ΔNp63β‐miR‐205 axis in epithelial–mesenchymal transition of oral squamous cell carcinoma via targeting ZEB1 and ZEB2 下载免费PDF全文
Yuma Hashiguchi Shintaro Kawano Yuichi Goto Kaori Yasuda Naoki Kaneko Taiki Sakamoto Ryota Matsubara Teppei Jinno Yasuyuki Maruse Hideaki Tanaka Masahiko Morioka Taichi Hattori Shoichi Tanaka Tamotsu Kiyoshima Seiji Nakamura 《Journal of cellular physiology》2018,233(10):6565-6577
We previously revealed that epithelial‐to‐mesenchymal transition (EMT) was mediated by ΔNp63β, a splicing variant of ΔNp63, in oral squamous cell carcinoma (OSCC). Recent studies have highlighted the involvement of microRNA (miRNA) in EMT of cancer cells, though the mechanism remains unclear. To identify miRNAs responsible for ΔNp63β‐mediated EMT, miRNA microarray analyses were performed by ΔNp63β‐overexpression in OSCC cells; SQUU‐B, which lacks ΔNp63 expression and displays EMT phenotypes. miRNAs microarray analyses revealed miR‐205 was the most up‐regulated following ΔNp63β‐overexpression. In OSCC cells, miR‐205 expression was positively associated with ΔNp63 and negatively with zinc‐finger E‐box binding homeobox (ZEB) 1 and ZEB2, potential targets of miR‐205. miR‐205 overexpression by miR‐205 mimic transfection into SQUU‐B cells led to decreasing ZEB1, ZEB2, and mesenchymal markers, increasing epithelial markers, and reducing cell motilities, suggesting inhibition of EMT phenotype. Interestingly, the results opposite to this phenomenon were obtained by transfection of miR‐205 inhibitor into OSCC cells, which express ΔNp63 and miR‐205. Furthermore, target protector analyses revealed direct regulation by miR‐205 of ZEB1 and ZEB2 expression. These results showed tumor‐suppressive roles of ΔNp63β and miR‐205 by inhibiting EMT thorough modulating ZEB1 and ZEB2 expression in OSCC. 相似文献
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Tannic acid attenuates TGF‐β1‐induced epithelial‐to‐mesenchymal transition by effectively intervening TGF‐β signaling in lung epithelial cells 下载免费PDF全文
Dhamotharan Pattarayan Ayyanar Sivanantham Venkateshwaran Krishnaswami Lakshmanan Loganathan Rajaguru Palanichamy Subramanian Natesan Karthikeyan Muthusamy Subbiah Rajasekaran 《Journal of cellular physiology》2018,233(3):2513-2525