MicroRNA‑466 inhibits osteosarcoma cell proliferation and induces apoptosis by targeting CCND1

Cao, Wei; Fang, Le; Teng, Siyong; Chen, Hongwei; Liu, Tiejun

doi:10.3892/etm.2018.6888

Cited by 9 publications

(10 citation statements)

References 29 publications

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“…miR-466 has been shown to be a tumor suppressor in osteosarcoma ( 31 ) and colorectal cancer ( 32 ). miR-466 regulates its target gene RUNX2 to inhibit bone metastasis and tumor growth in prostate cancer ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

Sun

Wang

Ding

et al. 2020

Braz J Med Biol Res

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LINC00355 has been reported aberrantly over-expressed and associated with poor prognosis in various types of cancer. However, reports regarding the effect of LINC00355 on lung squamous cell carcinoma (SCC) are rare. This study aimed to explore the function of LINC00355 in the development and progression of lung SCC and reveal the underlying mechanism. The expression and subcellular location of LINC00355 were determined by qRT-PCR and RNA-FISH, respectively. The lung SCC cell growth was analyzed by CCK-8 assay, transwell invasion, wound healing, colony formation, and flow cytometry assays. Reactive oxygen species level was evaluated by DCFH-DA probes. Bioinformatics online websites, luciferase reporter assay, RNA binding protein immunoprecipitation (RIP), and RNA pull-down assays were utilized to investigate the interaction among LINC00355, miR-466, and Ly-1 antibody reactive clone (LYAR). The results showed that LINC00355 was upregulated in lung SCC and was positively associated with poor overall survival in lung SCC patients. LINC00355 was mainly located in the cytoplasm of SCC cells. Additionally, LINC0035 functioned as a competing endogenous RNA (ceRNA) to target miR-466, and LYAR was identified as a direct target of miR-466. LINC00355 expression negatively correlated with miR-466 level, and positively correlated with LYAR level. Mechanistically, knockdown of LINC00355 inhibited cell proliferation, migration and invasion, promoted cell apoptosis in vitro , and suppressed tumor growth in vivo through targeting miR-466, and thus down-regulated LYAR expression. These findings provide a new sight for understanding the molecular mechanism of lung SCC and indicate that LINC00355 may serve as a potential biomarker for the diagnosis and treatment of lung SCC.

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Section: Discussionmentioning

confidence: 99%

LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

Sun

Wang

Ding

et al. 2020

Braz J Med Biol Res

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“…Our data showed all the proliferation-related genes appeared to be up-regulated after the CYP19A1 knockdown. Previous studies have demonstrated that all of them play important regulatory roles in cell proliferation and the cell cycle (21)(22)(23)(24). For example (25), found that neuron growth factors (NGF) promote the proliferation of granulosa cells (GC) by downregulating ESR2 and CDKN1A.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

Duan

et al. 2020

Front. Vet. Sci.

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Cytochrome P450 aromatase 19A1 (CYP19A1) is a critical enzyme in estrogen synthesis. However, the effect of CYP19A1 on cell growth and hormone secretion of buffalo follicular granulosa cells (BFGCs) is poorly understood. The objective of this study was to assess the role of CYP19A1 in cell proliferation and hormone secretion of BFGCs by knocking down CYP19A1 mRNA expression. The mRNA expression level of CYP19A1 gene was knocked down in BFGCs using the siCYP19A1-296 fragment with the best interference efficiency of 72.63%, as affirmed by real-time quantitative PCR (qPCR) and cell morphology analysis. The CYP19A1 knockdown promoted the proliferation of BFGCs through upregulating the mRNA expression levels of six proliferation-related genes (CCND1, CCNE1, CCNB1, CDK2, CDKN1A, and CDKN1B). Moreover, CYP19A1 knockdown increased (P < 0.05) the concentrations of progesterone secretion (P4) in BFGCs through increasing the mRNA expression levels of three steroidogenic genes (HSD17B1, HSD17B7, and CYP17A1). Our data further found that the FSH could inhibit the mRNA expression level of CYP19A1 in BFGCs, while LH obtains the opposite effect. These findings showed that the CYP19A1 knockdown had a regulatory role in the hormone secretion and cell proliferation in BFGCs.

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“…Herein, we found that miR‐466 was abundantly bound by PGM5‐AS1, as demonstrated by RNA pull‐down and luciferase reporter assays. miR‐466 was reported as a tumor suppressor in osteosarcoma, colorectal cancer, and prostate cancer, while as an oncogene in cervical cancer, implying that miR‐466 is expressed in a disease‐or tissue‐specific manner. However, its role in ESCC remains unknown.…”

Section: Discussionmentioning

confidence: 99%

p53‐induced long non‐coding RNA PGM5‐AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR‐466/PTEN axis

et al. 2019

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A growing body of evidence suggests that long non‐coding RNA (lncRNA) is aberrantly expressed in human cancer and linked to cancer initiation and development. We previously identified Homo sapiens PGM5 antisense RNA 1 (PGM5‐AS1) as a novel esophageal squamous cell carcinoma (ESCC)‐related lncRNA by performing high‐throughput RNA sequencing. However, its clinical implication and biological function in ESCC are still uncharacterized. In the present study, we found that PGM5‐AS1 was frequently downregulated in ESCC tissues, plasma, and cell lines, and low PGM5‐AS1 expression was positively correlated with poor differentiation, advanced tumor node metastasis (TNM) stage, and lymph node metastasis. Importantly, PGM5‐AS1 was identified to be an effective diagnostic and prognostic biomarker for ESCC patients. Functional experiments revealed that exogenous expression of PGM5‐AS1 significantly suppressed the proliferation, migration, and invasion of ESCC cells in vitro as well as tumor growth in vivo. Mechanistically, PGM5‐AS1 was transcriptionally activated by p53 and it could directly interact with and sequester miR‐466 to elevate PTEN expression, thereby inhibiting ESCC progression. Overall, our data indicate that PGM5‐AS1 is a novel tumor suppressor in ESCC and restoration of PGM5‐AS1 may be a promising avenue for treatment of ESCC patient.

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MicroRNA‑466 inhibits osteosarcoma cell proliferation and induces apoptosis by targeting CCND1

Cited by 9 publications

References 29 publications

LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

p53‐induced long non‐coding RNA PGM5‐AS1 inhibits the progression of esophageal squamous cell carcinoma through regulating miR‐466/PTEN axis

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