MiR-93-5p promotes gastric cancer-cell progression via inactivation of the Hippo signaling pathway

Li, Li; Zhao, Jinmin; Huang, Shanshan; Wang, Yi; Zhu, Lijing; Cao, Yuan; Xiong, Jianping; Deng, Jun

doi:10.1016/j.gene.2017.09.071

Cited by 56 publications

(40 citation statements)

References 32 publications

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“…It has been suggested that miR-93-5p plays an oncogenic role in multiple tumors. For example, according to a previous report, miR-93-5p is expressed highly in GC tissues and could promote the development of GC through the inactivation of the Hippo signaling pathway [21]. Besides GC, the proliferation and migration of non-small cell lung cancer (NSCLC) cells can also be regulated by miR-93-5p, while up-regulation of miR-93-5p results in poor prognosis of NSCLC by binding with the 3′-untranslated region of the tumor suppressor gene PTEN and RB1 [22].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-93-5p promotes epithelial-mesenchymal transition in gastric cancer by repressing tumor suppressor AHNAK expression

et al. 2020

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Background: Gastric cancer (GC) is a common cause of cancer-related mortality worldwide, and microRNAs (miRNAs) have been shown to play an important role in GC development. This study aims to explore the effect of microRNA-93-5p (miR-93-5p) on the epithelial-mesenchymal transition (EMT) in GC, via AHNAK and the Wnt signaling pathway. Methods: Microarray-based gene expression analysis was performed to identify GC-related differentially expressed miRNAs and genes. Then the expression of the miR-93-5p was examined in GC tissues and GC cell lines. The targeting relationship between miR-93-5p and AHNAK was verified by a dual luciferase reporter gene assay. In an attempt to ascertain the contributory role of miR-93-5p in GC, miR-93-5p mimic or inhibitor, as well as an AHNAK overexpression vector, were introduced to HGC-27 cells. HGC-27 cell migration and invasive ability, and EMT were assayed using Transwell assay and western blot analysis. Regulation of the Wnt signaling pathway was also assessed using TOP/FOP flash luciferase assay. Results: miR-93-5p was highly expressed in GC tissue samples and cells. Notably, miR-93-5p could target and negatively regulate AHNAK. Down-regulation of miR-93-5p or overexpression of AHNAK could suppress the migration and invasion abilities, in addition to EMT in GC cells via inactivation of the Wnt signaling pathway. Conclusion: Taken together, downregulation of miR-93-5p attenuated GC development via the Wnt signaling pathway by targeting AHNAK. These findings provide an enhanced understanding of miR-93-5p as a therapeutic target for GC treatment.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-93-5p promotes epithelial-mesenchymal transition in gastric cancer by repressing tumor suppressor AHNAK expression

et al. 2020

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“…The results indicated that in SW480 cells, miR‐93‐5p regulated PD‐L1 specifically and negatively, which was previously found in pancreatic cancer (Cioffi et al, 2017); moreover, we also noted that transfection of miR‐93‐5p mimics decreased the level of PD‐L1, and this effect was abolished with the administration of inhibitors; in PD‐L1‐negative patients, miR‐93‐5p expression was significantly elevated, suggesting the key role of miR‐93‐5p targeting PD‐L1 . miR‐93‐5p, a member of the miR‐106b‐25 gene cluster located on chromosome 7q22, is not only an oncogene in many tumors (Li et al, 2018, 2019) but is also a tumor suppressor in certain tumors (Shyamasundar et al, 2016; Xiang et al, 2017). The results of this study suggested that miR‐93‐5p expression was downregulated in the tumor tissues and had a significant association with the major clinicopathological features and survival of patients.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐93‐5p expression in tumor tissue and its tumor suppressor function via targeting programmed death ligand‐1 in colorectal cancer

Chen

Wang

Lin

et al. 2020

Cell Biology International

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This work aimed to investigate miR-93-5p expression in tumor tissue and its in vitro effects in colorectal cancer (CRC) by targeting programmed death ligand-1 (PD-L1). MiR-93-5p and PD-L1 expression was detected in CRC and adjacent normal tissues by quantitative real-time polymerase chain reaction and immunohistochemistry. The correlation between miR-93-5p and PD-L1 was validated by a dual-luciferase reporter assay. HCT116 and SW480 cells were divided into blank, miR-NC, miR-93-5p mimics, miR-93-5p inhibitor, PD-L1 small interfering RNA (siRNA) and miR-93-5p inhibitor + PD-L1 siRNA groups, and wound-healing and transwell assays were performed to detect cell migration and invasion, respectively. Protein expression was measured by western blotting. The secretion of cytokines was detected in the CRC cell/T coculture models. MiR-93-5p was downregulated in CRC tissues with upregulated PD-L1. In PD-L1-negative patients, miR-93-5p expression was increased compared with that in PD-L1-positive patients. MiR-93-5p and PD-L1 expression levels were associated with the tumor differentiation, lymphatic metastasis, TNM, Duke's stage, and prognosis of CRC. PD-L1 siRNA weakened the migration and invasion abilities via decreased expression of matrix metalloproteinase-1 (MMP-1), -2, and -9, and these effects were abolished by the miR-93-5p inhibitor. Additionally, anti-PD-L1 upregulated the expressions of interleukin-2 (IL-2), tumor necrosis factor-α (TNF-α), and interferon γ (IFN-γ) in the coculture of T cells with CRC cells, but downregulated the expressions of IL-1β, IL-10, and TGF-β. However, these changes were partially reversed by miR-93-5p inhibition. miR-93-5p is expected to be a novel target for CRC treatment since it decreases the migration and invasion, as well as the immune evasion, of CRC cells via targeting PD-L1. Abbreviations: CRC, colorectal cancer; ELISA, enzyme-linked immunosorbent assay; HE, hematoxylin and eosin; ITIM, immunoreceptor tyrosinebased inhibitory motif; miRNA, microRNA; PD-L1, programmed death ligand-1 Role of miR-93-5p in CRC via targeting PD-L1Y.-L. Chen et al.

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“…miR-93-5p has been demonstrated to serve as an oncogene and promote tumor growth and metastasis in numerous types of cancer, including ovarian carcinoma (30), endometrial carcinoma (31), triple-negative breast cancer (32), gastric cancer (19), non-small cell lung cancer (11) and hepatocellular carcinoma (18). However, to the best of our knowledge, the physiological functions and underlying molecular mechanism of miR-93-5p in RB have not been investigated.…”

Section: Discussionmentioning

confidence: 99%

“…miR-93-5p has been recently reported to promote the proliferation and metastasis of numerous human cancers, including hepatocellular carcinoma (18), non-small cell lung cancer (11) and gastric cancer (19); however, the functions of miR-93-5p in RB remain elusive. In the present study, it was revealed that miR-93-5p expression was significantly upregulated in RB tissues compared with in normal tissues.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

et al. 2018

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Numerous repor ts have indicated that microRNA-93-5p (miR-93-5p) is involved in the development and progression of human cancer, including non-small cell lung, gastric and breast cancer; however, the role of miR-93-5p in retinoblastoma (RB) remains unknown. In the present study, it was reported that miR-93-5p expression levels were significantly upregulated in RB tissues compared with in normal tissues by reverse transcription-quantitative polymerase chain reaction. Furthermore, it was demonstrated via cell counting kit-8 and Transwell assays that knockdown of miR-93-5p significantly suppressed the proliferation, migration and invasion of RB cells, but promoted cellular apoptosis. Regarding the underlying mechanism, the present study reported that phosphatase and tensin homolog (PTEN) was a direct target of miR-93-5p in RB cells. Overexpression of miR-93-5p significantly inhibited the expression of PTEN; opposing results were observed when PTEN expression was downregulated. Furthermore, the present study revealed that PTEN expression levels were downregulated and were inversely correlated with that of miR-93-5p in RB tissues. Additionally, the present study demonstrated that knockdown of PTEN in miR-93-5p-depleted RB cells significantly reversed the effects of miR-93-5p on cell proliferation, migration and invasion; miR-93-5p knockdown was suggested to promote PTEN expression, consequently inhibiting the activation of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Collectively, the results of the present study demonstrated that miR-93-5p may serve a role as an oncogene by modulating the PTEN/PI3K/AKT signaling pathway in RB, indicating that miR-93-5p may be a potential therapeutic target for the treatment of RB.

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MiR-93-5p promotes gastric cancer-cell progression via inactivation of the Hippo signaling pathway

Cited by 56 publications

References 32 publications

RETRACTED ARTICLE: MicroRNA-93-5p promotes epithelial-mesenchymal transition in gastric cancer by repressing tumor suppressor AHNAK expression

RETRACTED ARTICLE: MicroRNA-93-5p promotes epithelial-mesenchymal transition in gastric cancer by repressing tumor suppressor AHNAK expression

MicroRNA‐93‐5p expression in tumor tissue and its tumor suppressor function via targeting programmed death ligand‐1 in colorectal cancer

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

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