Regulation of cell proliferation and migration in gallbladder cancer by zinc finger X-chromosomal protein

Tan, Zhen; Zhang, Shenglai; Li, Maolan; Wu, Xiangsong; Weng, Hao; Ding, Qi; Yang, Cao; Bao, Runfa; Shu, Yijun; Mu, Jian; Ding, Qichen; Wu, Wenzhi; Yang, Jingsi; Zhang, Lin; Liu, Yingbin

doi:10.1016/j.gene.2013.06.064

Cited by 26 publications

(22 citation statements)

References 26 publications

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“…Recently, ZFX was shown to be involved in various physiological functions, including proliferation, differentiation, cell cycle, and cell death [23], and ZFX is highly expressed in malignant tumors, such as renal carcinoma, gastric carcinoma, and colorectal cancer [24–26]. In previous studies, we demonstrated that ZFX expression was significantly correlated with clinical biological behaviors and represented a significant prognostic marker for total post-operative survival in GBC [27, 28]. In the present study, we demonstrated using a luciferase reporter assay that miR-101 could bind to a sequence within the 3′UTR of ZFX.…”

Section: Discussionmentioning

confidence: 99%

miR-101 targeting ZFX suppresses tumor proliferation and metastasis by regulating the MAPK/Erk and Smad pathways in gallbladder carcinoma

Bao

Shu

et al. 2016

Oncotarget

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Gallbladder cancer (GBC), the most common malignancy of the bile duct, is highly aggressive and has an extremely poor prognosis, which is a result of early metastasis. As it is regulated being at multiple levels, the metastatic cascade in GBC is complex. Recent evidence suggests that microRNAs (miRNAs) are involved in cancer metastasis and are promising therapeutic targets. In this study, miR-101 was significantly downregulated in tumor tissues, particularly in metastatic tissues. In GBC patients, low miR-101 expression was correlated with tumor size, tumor invasion, lymph node metastasis, TNM stage, and poor survival. Moreover, miR-101 was an independent prognostic marker for GBC. Additionally, miR-101 inhibited GBC cell proliferation, migration, invasion, and TGF-β-induced epithelial-mesenchymal transition (EMT) in vitro and in vivo. Mechanistically, the gene encoding the zinc finger protein X-linked (ZFX) was identified as a direct target of miR-101. More importantly, miR-101 significantly reduced activation of the MAPK/Erk and Smad signaling pathways, resulting in inhibition of TGF-β-mediated induction of EMT. Altogether, our findings demonstrate a novel mechanism by which miR-101 attenuates the EMT and metastasis in GBC cells and suggest that miR-101 can serve as a potential biomarker and therapeutic target for GBC management.

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Section: Discussionmentioning

confidence: 99%

miR-101 targeting ZFX suppresses tumor proliferation and metastasis by regulating the MAPK/Erk and Smad pathways in gallbladder carcinoma

Bao

Shu

et al. 2016

Oncotarget

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“…The process of tumor development requires multiple steps, including cell initiation, proliferation, invasion and metastasis [17,18]. We have previously identified several other medicines that inhibit tumor cell proliferation and induce apoptosis, thereby influencing the process of tumor development [17,19].…”

Section: Discussionmentioning

confidence: 99%

Ursolic acid induces cell cycle arrest and apoptosis of gallbladder carcinoma cells

Weng

Tan

et al. 2014

Cancer Cell Int

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BackgroundUrsolic acid (UA), a plant extract used in traditional Chinese medicine, exhibits potential anticancer effects in various human cancer cell lines in vitro. In the present study, we evaluated the anti-tumoral properties of UA against gallbladder carcinoma and investigated the potential mechanisms responsible for its effects on proliferation, cell cycle arrest and apoptosis in vitro.MethodsThe anti-tumor activity of UA against GBC-SD and SGC-996 cells was assessed using MTT and colony formation assays. An annexin V/PI double-staining assay was used to detect cell apoptosis. Cell cycle changes were detected using flow cytometry. Rhodamine 123 staining was used to assess the mitochondrial membrane potential (ΔΨm) and validate UA’s ability to induce apoptosis in both cell lines. The effectiveness of UA in gallbladder cancer was further verified in vivo by establishing a xenograft GBC model in nude mice. Finally, the expression levels of cell cycle- and apoptosis-related proteins were analyzed by western blotting.ResultsOur results suggest that UA can significantly inhibit the growth of gallbladder cancer cells. MTT and colony formation assays indicated dose-dependent decreases in cell proliferation. S-phase arrest was observed in both cell lines after treatment with UA. Annexin V/PI staining suggested that UA induced both early and late phases of apoptosis. UA also decreased ΔΨm and altered the expression of molecules regulating the cell cycle and apoptosis. In vivo study showed intraperitoneally injection of UA can significantly inhibited the growth of xenograft tumor in nude mice and the inhibition efficiency is dose related. Activation of caspase-3,-9 and PARP indicated that mitochondrial pathways may be involved in UA-induced apoptosis.ConclusionsTaken together, these results suggest that UA exhibits significant anti-tumor effects by suppressing cell proliferation, promoting apoptosis and inducing 7cell cycle arrest both in vitro and in vivo. It may be a potential agent for treating gallbladder cancer.

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“…Recently, ZFX has been found to be overexpressed in different cancer types [14][15][16][17][18][19] . Inhibition of ZFX expression in different cancer cells by RNAi resulted in significantly impaired cell proliferation, increased apoptosis, and arrest in the G1 phase of the cell cycle [20][21][22][23] .…”

Section: Introductionmentioning

confidence: 99%

Differential Expression Profile of ZFX Variants Discriminates Breast Cancer Subtypes

Pourkeramati¹,

Asadi²,

Shakeri³

et al. 2019

ibj

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Background: ZFX is a transcriptional regulator in embryonic stem cells and plays an important role in pluripotency and self-renewal. ZFX is widely expressed in pluripotent stem cells and is down-regulated during differentiation of embryonic stem cells. ZFX has five different variants that encode three different protein isoforms. While several reports have determined the overexpression of ZFX in a variety of somatic cancers, the expression of ZFX-spliced variants in cancer cells is not well-understood. Methods: We investigated the expression of ZFX variants in a series of breast cancer tissues and cell lines using quantitative PCR. Results: The expression of ZFX variant 1/3 was higher in tumor tissue compared to marginal tissue. In contrast, the ZFX variant 5 was down-regulated in tumor tissues. While the ZFX variant 1/3 and ZFX variant 5 expression significantly increased in low-grade tumors, ZFX variant 4 was strongly expressed in high-grade tumors, demonstrating lymphatic invasion. In addition, our result revealed a significant association between the HER2 status and the expression of ZFX-spliced variants. Conclusion: Our data suggest that the expression of ZFX-spliced transcripts varies between different types of breast cancer and may contribute to their tumorigenesis process. Hence, ZFX-spliced transcripts could be considered as novel tumor markers with a probable value in diagnosis, prognosis, and therapy of breast cancer.

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Regulation of cell proliferation and migration in gallbladder cancer by zinc finger X-chromosomal protein

Cited by 26 publications

References 26 publications

miR-101 targeting ZFX suppresses tumor proliferation and metastasis by regulating the MAPK/Erk and Smad pathways in gallbladder carcinoma

miR-101 targeting ZFX suppresses tumor proliferation and metastasis by regulating the MAPK/Erk and Smad pathways in gallbladder carcinoma

Ursolic acid induces cell cycle arrest and apoptosis of gallbladder carcinoma cells

Differential Expression Profile of ZFX Variants Discriminates Breast Cancer Subtypes

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