<i>Retracted:</i> miR‐518b is down‐regulated, and involved in cell proliferation and invasion by targeting Rap1b in esophageal squamous cell carcinoma

Zhang, Mingxin; Zhou, Suna; Zhang, Ling-min; Jia, Zhang; Cai, Hui; Jin-xiang, Zhu; Huang, Chen; Wang, Jiansheng

doi:10.1016/j.febslet.2012.08.007

Cited by 61 publications

(50 citation statements)

References 26 publications

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“…Individual miRNAs each have several hundred different target genes, including oncogenes and anti-oncogenes. The function of a miRNA is not dependent on a single target gene, but rather on the competition or balance among its target genes in specific types of cancer (32). Therefore, there may be a balanced relationship among the oncogenes or tumor suppressor target genes of miR-126 in SGC-7901 cells.…”

Section: Discussionmentioning

confidence: 99%

miR-126 inhibits growth of SGC-7901 cells by synergistically targeting the oncogenes PI3KR2 and Crk, and the tumor suppressor PLK2

Liu

Wang

Zhao

et al. 2014

International Journal of Oncology

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Abstract. MicroRNA (miRNA)-126 (miR-126) was reported to be downregulated and to act as a tumor suppressor in cancers of the lung, cervix, bladder and prostate. However, the functions of miR-126 in gastric cancer appear to be diverse and are largely unknown. MiR-126 was reported to act as a tumor suppressor by targeting the Crk gene, or as an oncogene by targeting the SOX2 gene in gastric cancer. We identified that the expression of miR-126 was decreased in gastric cancer cell lines and tissues. PLK2, a tumor suppressor gene, was directly regulated by miR-126 in SGC-7901 cells. Overexpression of miR-126 not only suppressed the growth and clone formation of SGC-7901 cells, but also induced apoptosis in vitro, whereas inhibition of miR-126 slightly promoted SGC-7901 cell proliferation. The cell cycle was not affected by miR-126. Moreover, miR-126 suppressed tumor growth in vivo in a xenograft model. PLK2, PI3KR2and Crk were regulated by miR-126 in SGC-7901 cells. We infer that the functions of miR-126 in gastric cancer depend on synergistic targeting balance between oncogenes and anti-oncogenes. Our study indicates that miR-126 is a tumor suppressor, which in the future may become a therapeutic target for gastric cancer.

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Section: Discussionmentioning

confidence: 99%

miR-126 inhibits growth of SGC-7901 cells by synergistically targeting the oncogenes PI3KR2 and Crk, and the tumor suppressor PLK2

Liu

Wang

Zhao

et al. 2014

International Journal of Oncology

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“…It has been reported that miR-21, miR-106b, miR-373, miR-192, miR-196a and miR-147 were upregulated in patients with ESCC (26)(27)(28)(29)(30), suggesting that they may exert tumor oncogene functions, while miR-655, miR-375, miR-625, miR-518b, miR-133a, miR-133b, miR-143 and miR-145 were downregulated in patients with ESCC (26,29,(31)(32)(33), suggesting that they may exert tumor suppressive functions. Here, we sought to provide evidence that upregulation of miR-218 inhibits tumor growth of ESCC in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

miR-218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin

et al. 2014

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Abstract.A growing body of evidence suggests that microRNA-218 (miR-218) acts as a tumor suppressor and is involved in tumor progression, development and metastasis and confers sensitivity to certain chemotherapeutic drugs in several types of cancer. However, our knowledge concerning the exact roles played by miR-218 in esophageal squamous cell carcinoma (ESCC) and the underlying molecular mechanisms remain relatively unclear. Thus, the aims of this study were to detect the expression of miR-218 in human ESCC tissues and explore its effects on the biological features and chemosensitivity to cisplatin (CDDP) in an ESCC cell line (Eca109), so as to provide new insights for ESCC treatment. Here, we found increased expression of miR-218 in the ESCC tissues compared with that in the matched non-tumor tissues, and its expression level was correlated with key pathological characteristics including clinical stage, tumor depth and metastasis. We also found that enforced expression of miR-218 significantly decreased cell proliferation, colony formation, migration and invasion, induced cell apoptosis and arrested the cell cycle in the G0/G1 phase, as well as suppressed tumor growth in a nude mouse model. In addition, our results showed that miR-218 mimics increased the sensitivity to the antitumor effect of CDDP in the human Eca109 cells. Importantly, this study also showed that miR-218 regulated the expression of phosphorylated PI3K, AKT and mTOR, which may contribute to suppressed tumor growth of ESCC and enhanced sensitivity of ESCC cells. These findings suggest that miR-218 is a potential therapeutic agent for the treatment of ESCC.

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“…RAP1B, a Ras-related small GTP-binding protein that behaves as a GTPase, has been implicated as an oncogene in a variety of tumors, including esophageal squamous cell carcinoma (ESCC), CRC, T-acute lymphoblastic leukemia, non-small cell lung carcinoma, glioma and thyroid carcinoma [19–27]. RAP1B activates multiple signaling cascades associated with tumor development and progression and is involved in cell proliferation, invasion, cell adhesion and angiogenesis [19–29].…”

Section: Introductionmentioning

confidence: 99%

miR-28-5p acts as a tumor suppressor in renal cell carcinoma for multiple antitumor effects by targeting RAP1B

Wang

Yang

et al. 2016

Oncotarget

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The incidence and mortality rate of renal cell carcinoma (RCC) have been significantly increasing; however, the mechanisms involved in RCC development and progression are unclear. In this study, we found that miR-28-5p was decreased in RCC tumor specimens and several renal carcinoma cell lines. By using a combination of luciferase reporter assays and western blotting, we identified RAP1B, a Ras-related small GTP-binding oncoprotein implicated in a variety of tumors, as a direct target of miR-28-5p in RCC. The RAP1B protein level was increased in RCC tumor specimens and renal carcinoma cell lines, and this was inversely correlated with miR-28-5p expression. In vitro gain-of-function and loss-of-function studies in human renal carcinoma cell lines, demonstrated that miR-28-5p suppressed cell proliferation and migration by directly inhibiting RAP1B, and this effect was reversed by co-transfection with RAP1B. In addition, the stable overexpression of miR-28-5p inhibited tumor cell proliferation in vivo. This newly identified miR-28-5p/RAP1B axis provides a novel mechanism for the pathogenesis of RCC, and molecules in this axis may serve as potential biomarkers and therapeutic targets for RCC.

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Retracted: miR‐518b is down‐regulated, and involved in cell proliferation and invasion by targeting Rap1b in esophageal squamous cell carcinoma

Cited by 61 publications

References 26 publications

miR-126 inhibits growth of SGC-7901 cells by synergistically targeting the oncogenes PI3KR2 and Crk, and the tumor suppressor PLK2

miR-126 inhibits growth of SGC-7901 cells by synergistically targeting the oncogenes PI3KR2 and Crk, and the tumor suppressor PLK2

miR-218 suppresses tumor growth and enhances the chemosensitivity of esophageal squamous cell carcinoma to cisplatin

miR-28-5p acts as a tumor suppressor in renal cell carcinoma for multiple antitumor effects by targeting RAP1B

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