Identification of miR-125a-5p as a tumor suppressor of renal cell carcinoma, regulating cellular proliferation, migration and apoptosis

Chen, Duqun; Li, Yifan; Su, Zhengming; Yu, Zuhu; Yu, Wenshui; Li, Yuchi; Gui, Yaoting; Yang, Shangqi; Lai, Yongqing

doi:10.3892/mmr.2014.2848

Cited by 21 publications

(17 citation statements)

References 28 publications

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“…Current research on miR-222-5p has focused on the role of angiogenesis in the endothelium [21,22], and few studies investigated the effect of miR-222-5p in cancers. As down-regulated miRNAs in GAC, miR-125-5p was identified as a tumor suppressor in glioblastoma [23], cervical cancer [24], and renal cell carcinoma [25], which was involved in proliferation, migration, and apoptosis. More researches have investigated the role of miR-145-3p in cancers, such as bladder cancer [26], lung squamous cell carcinoma [27], gallbladder cancer [28], and head and neck squamous cell carcinoma [29], which is also considered as a tumor suppressor.…”

Section: Discussionmentioning

confidence: 99%

miR-96-5p enhances cell proliferation and invasion via targeted regulation of ZDHHC5 in gastric cancer

Wang¹,

Liu

Meng

2020

Bioscience Reports

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Objective: To explore the biological function and mechanism of miR-96-5p in gastric cancer. Methods: The expression of differently expressed microRNAs (DEMs) related to gastric adenocarcinoma (GAC) prognosis was identified in GAC tumor samples and adjacent normal samples by qRT-PCR. A target gene miR-96-5p was selected using TargetScan, miRTarBase, miRDB databases. The combination of miR-96-5p and ZDHHC5 was verified by luciferase receptor assay. To further study the function and mechanism of miR-96-5p, we treated MGC-803 cells with miR-96-5p inhibitor and si-ZDHHC5, then detected cell viability, apoptosis, migration and invasion ability, as well as the expression of ZDHHC5, Bcl-2, Bax, cleaved caspase-3, cleaved caspase-9, and COX-2 by Western blot. Results: Compared with adjacent normal samples, the levels of miR-96-5p, miR-222-5p, and miR-652-5p were remarkably increased, while miR-125-5p, miR-145-3p, and miR-379-3p were significantly reduced in GAC tumor samples (P<0.01), which were consistent with bioinformatics analysis. Furthermore, ZDHHC5 was defined as a direct target gene of miR-96-5p. miR-96-5p silence significantly reduced cell viability, increased cell apoptosis, and suppressed cell migration and invasion, as well as inhibited the expression of Bcl-2 and COX-2 and promoted Bax, cleaved caspase-3 and cleaved caspase-9 level in MGC-803 cells (P<0.01). Notably, ZDHHC5 silence reversed the inhibiting effects of miR-96-5p on MGC-803 cells growth and metastasis Conclusion: Our findings identified six microRNAs (miRNAs; miR-96-5p, miR-222-5p, miR-652-5p, miR-125-5p, miR-145-3p, and miR-379-3p) related to GAC prognosis, and suggested that down-regulated miR-96-5p might inhibit tumor cell growth and metastasis via increasing ZDHHC5 expression enhance MGC-803 cell apoptosis, as well as decrease MGC-803 cell metastasis.

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Section: Discussionmentioning

confidence: 99%

miR-96-5p enhances cell proliferation and invasion via targeted regulation of ZDHHC5 in gastric cancer

Wang¹,

Liu

Meng

2020

Bioscience Reports

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“…OC cell lines were cultured as described above, and ~5x10 6 OVCAR3 and HO8910 cells per well were cultured in 6-well plates at 37˚C and transfected with 100 nM siMALAT1 or siNC within 24 h using Lipofectamine ® 2000 reagent (Invitrogen; Thermo Fisher Scientific, Inc.) according to the manufacturer's protocol. Flow cytometry was performed as previously described (21). At 48 h post-transfection, cells were collected using trypsin reagent (Sigma-Aldrich, Merck KGaA, Darmstadt, Germany) and washed three times with cold PBS, then re-suspended in 100 µl of 1X binding buffer (Invitrogen; Thermo Fisher Scientific, Inc.).…”

Section: Tissuementioning

confidence: 99%

Long non-coding RNA MALAT1 is upregulated and involved in cell proliferation, migration and apoptosis in ovarian cancer

Wang

Guo

2017

Experimental and Therapeutic Medicine

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Abstract. Ovarian cancer (OC) is the leading cause of mortality among gynecological malignancies. Although microRNAs are known to have a key regulatory role in OC, the involvement of long non-coding RNAs in the disease is less established. Previous studies have demonstrated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a tumor oncogene in many cancers, though its role in OC remains unclear. The present study reported that MALAT1 expression was markedly upregulated in OC, by knockdown of MALAT1 expression in vivo, using RNA interference (RNAi) with small-interfering RNA (siRNA). It was found that MALAT1 expression was positively correlated with the International Federation of Gynecology and Obstetrics stages of OC, tumor histological grade and lymph node metastasis. In addition, the differential MALAT1 levels between a human ovarian epithelial cell line (HOSE) and OC cell lines (ES-2, OVCAR3, SKOV3 and HO8910) were compared in vitro. Notably, MALAT1 was expressed to a high level in OC cells. Furthermore, exogenous knockdown of MALAT1 significantly repressed growth and migration of OC cells, and promoted their apoptosis. Collectively, the current findings suggest that upregulation of MALAT1 in OC may facilitate tumorigenesis and metastasis. Knockdown of MALAT1 expression has potential as a novel target for the diagnosis and therapy of OC.

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“…Renal cell carcinoma (RCC) accounts for ~3% of all adult malignancies and is the most common type of adult kidney cancer (1). The long-term prospects for patients with advanced RCC have improved; however, disease progression-free survival in the absence of debilitating side effects remains a work-in-progress (2).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-24-2 is associated with cell proliferation, invasion, migration and apoptosis in renal cell carcinoma

Jin

Nie

et al. 2017

Molecular Medicine Reports

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Micro (mi)RNAs are involved in multiple cellular processes, and alterations in miRNA expression have been demonstrated to lead to tumorigenesis. Previous microarray analysis revealed that miRNA (miR)‑24 was downregulated in renal cell carcinoma (RCC). Additionally, miR‑24 has been identified as an oncogene and tumor suppressor in various cancers. The present study assessed the expression levels of two stem‑loops of miR‑24, miR‑24‑1 and miR‑24‑2, in RCC tissues and paired healthy tissues by reverse transcription‑quantitative polymerase chain reaction. The results revealed that miR‑24‑2 was upregulated in RCC tissues and ACHN, 786‑O and 769P cell lines compared with healthy tissues and HEK‑293T cells, respectively, whereas miR‑24‑1 was almost absent in RCC and healthy kidney tissues. To investigate the role of miR‑24‑2 in RCC, a synthesized miR‑24‑2 mimic, negative control (NC), inhibitor or inhibitor NC was transfected into 786‑O and ACHN RCC cells, and cell proliferation, mobility and apoptosis assays were performed. The results of the present study revealed that miR‑24‑2 was associated with cell proliferation, migration, invasion and apoptosis, thus demonstrating that miR‑24‑2 may serve a role as an oncogene in RCC. Further studies are required to investigate the signaling pathways of miR‑24‑2, and the potential of miR‑24‑2 as a therapeutic target or biomarker for the early detection of RCC.

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Identification of miR-125a-5p as a tumor suppressor of renal cell carcinoma, regulating cellular proliferation, migration and apoptosis

Cited by 21 publications

References 28 publications

miR-96-5p enhances cell proliferation and invasion via targeted regulation of ZDHHC5 in gastric cancer

miR-96-5p enhances cell proliferation and invasion via targeted regulation of ZDHHC5 in gastric cancer

Long non-coding RNA MALAT1 is upregulated and involved in cell proliferation, migration and apoptosis in ovarian cancer

MicroRNA-24-2 is associated with cell proliferation, invasion, migration and apoptosis in renal cell carcinoma

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