MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4

Zhou, Wuyuan; Zou, Benkui; Liu, Lisheng; Cui, Kai; Gao, Jie; Yuan, Shuanghu; Cong, Ning

doi:10.18632/oncotarget.12190

Cited by 51 publications

(49 citation statements)

References 42 publications

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“…miR-98 is a tumor suppressive miRNA, knockdown of which leads to a reduction of 1,25-vitamin D anti-growth effect of prostate cancer and overexpression of miR-98 suppressed prostate cancer cell growth (23). miR-98 inhibits human ovarian cancer stem cell proliferation via retinoblastoma-associated protein-E2F transcription factor pathway and suppresses hepatocellular carcinoma by targeting Sal-like protein 4 and collagen triple helix repeat containing 1 (24)(25)(26). Currently, a limited amount of data is available regarding miR-98-mediated regulation of osteoblast differentiation.…”

Section: Discussionmentioning

confidence: 99%

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

et al. 2018

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Casein kinase 2-interacting protein 1 (CKIP-1) is a negative regulator for bone formation. Previously, using bioinformatics analysis, CKIP‑1 has been predicted to serve the role of target gene of miR‑98‑5p. In the present study, the potential role of miR‑98‑5p in regulating osteoblast differentiation through CKIP‑1 was investigated. Following pre‑treatment with microRNA (miR)‑98‑5p agomir or miR‑98‑5p antagomir, MC3T3‑E1 cells were cultured in an osteoinductive medium. Subsequently, the expression of miR‑98‑5p, CKIP‑1 and levels of osteoblast differentiation markers, including alkaline phosphatase, matrix mineralization, osteocaicin, collagen type I, runt‑related transcription factor 2 and osteopontin were assayed. Using a dual‑luciferase reporter assay, it was demonstrated that CKIP‑1 was the target gene of miR‑98‑5p. miR‑98‑5p was upregulated as a result of treatment with miR‑98‑5p agomir and promoted osteoblast differentiation. Conversely, miR‑98‑5p antagomir inhibited miR‑98‑5p expression and osteoblast differentiation. miR‑98‑5p targeted CKIP‑1 by binding to its 3'‑untranslated region. Furthermore, miR‑98‑5p overexpression decreased the protein levels of CKIP‑1 and inhibition of miR‑98‑5p increased the protein levels of CKIP‑1. The results of the present study indicated that CKIP‑1 was a target gene of miR‑98‑5p and that miR‑98‑5p regulated osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1.

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Section: Discussionmentioning

confidence: 99%

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

et al. 2018

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“…miRNAs function as specific gene regulators by interacting preferentially with the 3' untranslated region (3'UTR) of their target genes in a base-pairing manner, and subsequently inducing mRNA degradation or translational repression (7). To date, various miRNAs have been investigated that may serve important roles in diverse biological processes, such as cell proliferation, viability, apoptosis, cell cycle, angiogenesis, invasion, motility and differentiation (8)(9)(10). A previous study reported that >50% of known miRNAs are located at genomic regions or in fragile sites closely correlated with cancer (11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-302a inhibits cell proliferation and invasion, and induces cell apoptosis in hepatocellular carcinoma by directly targeting VEGFA

Qin

Zha

Fan

et al. 2017

Molecular Medicine Reports

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Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third most common cause of cancer‑related mortality worldwide. An increasing number of studies have demonstrated that microRNAs may be used as diagnostic, therapeutic and prognostic targets for human cancers, including HCC. The present study aimed to evaluate microRNA (miR)‑302a expression and function in HCC, and its underlying mechanisms. The results revealed that miR‑302a was expressed at low levels in HCC tissues and cell lines. Reduced miR‑302a expression was correlated with tumor‑node‑metastasis stage and lymph node metastasis in patients with HCC. Additionally, overexpression of miR‑302a reduced cell proliferation and invasion, and induced apoptosis in HCC cells. Vascular endothelial growth factor A (VEGFA) was demonstrated to be a direct target gene of miR‑302a. VEGFA was highly expressed in HCC tissues and inversely correlated with miR‑302a expression. Knockdown of VEGFA expression led to reduced HCC cell proliferation and invasion, and increased apoptosis rates, similar to miR‑302a overexpression, which suggested that VEGFA may be a functional downstream target of miR‑302a in HCC. These data suggested that this newly identified miR‑302a/VEGFA axis may be involved in HCC formation and progression. The present results also provide novel potential targets for the treatments of patients with HCC.

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“…Some of these mesenchymal markers also contribute to cell stemness, for example, Snail inducing CD44 high CD24 low CSC population 34 and ZEB1 inducing tumorinitiating capacity in pancreatic and colorectal cancer cells. 35 36 and esophageal squamous cell carcinoma. 37 Tian group predicted, through bioinformatics analysis that "GTGG" was one of the putative binding sites of SALL protein family.…”

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confidence: 99%

SALL4 promotes tumor progression in breast cancer by targeting EMT

Chen

Tsang

et al. 2020

Molecular Carcinogenesis

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Sal‐like protein 4 (SALL4) is overexpressed in breast cancer and might contribute to breast cancer progression, but the molecular mechanism remains unknown. Here, we found that within a group of 371 ethnic Chinese breast cancer patients, SALL4 was associated with lower grade (P = .002) and progesterone receptor positivity (P = .004) for overall cases; lower Ki67 (P = .045) and high vimentin (P = .007) for luminal cases. Patients with high SALL4 expression in lymph node metastasis showed a significantly worse survival than those with low expression. Knockout of SALL4 in a triple‐negative breast cancer cell line MDA‐MB‐231‐Red‐FLuc‐GFP led to suppressed ability in proliferation, clonogenic formation, migration, and mammosphere formation in vitro, tumorigenicity and lung colonization in vivo. On the other hand, overexpression of SALL4 enhanced migration and mammosphere formation in vitro and tumorigenicity in vivo. Mechanistically, there was a positive correlation between SALL4 expression and mesenchymal markers including Zinc finger E‐box binding homeobox 1 (ZEB1), vimentin, Slug, and Snail in vivo. Chromatin immunoprecipitation experiment indicated that SALL4 can bind to the promoter region of vimentin (−778 to −550 bp). Taken together, we hypothesize that SALL4 promotes tumor progression in breast cancer by inducing the mesenchymal markers like vimentin through directly binding to its promoter. Increased SALL4 level in metastatic lymph node relative to the primary site is an important poor survival marker in breast cancer.

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MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4

Cited by 51 publications

References 42 publications

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

MicroRNA-302a inhibits cell proliferation and invasion, and induces cell apoptosis in hepatocellular carcinoma by directly targeting VEGFA

SALL4 promotes tumor progression in breast cancer by targeting EMT

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