Increased expression of microRNA-148a in osteosarcoma promotes cancer cell growth by targeting PTEN

Zhang, Hao; Wang, Yan; Xu, Tianming; Li, Chen; Wu, Jiang; He, Qianyun; Wang, Guangchao; Ding, Chen; Liu, Kang; Tang, Hao; Ji, Fang

doi:10.3892/ol.2016.5050

Cited by 30 publications

(29 citation statements)

References 25 publications

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“…In addition, several miRNAs have been reported to be dysregulated in osteosarcoma 24 . As miR-422a inhibits the proliferation of osteosarcoma cells by targeting BCL2L2 and KRAS 25 , miR-148a promotes cancer cell growth in osteosarcoma by targeting phosphatase and tensin homolog (PTEN) 26 and miR-133a inhibits osteosarcoma progression by targeting Bcl-xL and Mcl-1 27 . In this study, we confirmed that miR-143 is the regulator of bone formation; thus, miR-143 is involved in both osteoblast differentiation and carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

et al. 2020

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The regulation of bone formation and detailed mechanisms are still largely elusive, and the roles of microRNAs in this process have attracted much attention. Recently, a specific subtype of CD31 hi endomucin hi (CD31 hi EMCN hi) endothelium has been identified to promote bone formation, together with osteoblast development. However, the role of microRNA143 in the generation of CD31 hi EMCN hi endothelium and bone formation remains unknown. In this study, we found that miR-143 was expressed both in osteoblast cells and CD31 hi EMCN hi endothelial cells. Serum miR-143 level was negatively correlated with age in humans. Overexpression of miR-143 promoted osteoblast formation and angiogenic effects. Furthermore, CD31 hi Emcn hi vessels and osteoblast formation were significantly inhibited in miR-143 knockout mice. Mechanistically, inhibitor HDAC7 was directly targeted by miR-143 and knockdown of HDAC7 was found to rescue the function of miR-143 deficiency. Thus, miR-143 promotes angiogenesis coupling with osteoblast differentiation by targeting HDAC7, which may serve as a potential target in angiogenic and osteogenic diseases.

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Section: Discussionmentioning

confidence: 99%

miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

et al. 2020

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“…Feng et al showed that microRNA-148a suppressed cell proliferation and migration of pancreatic cancer cells (6). Zhang et al showed that microRNA-148a suppressed cell proliferation and invasion potential through regulation of STAT3 in non-small cell lung carcinomas (7).…”

Section: Introductionmentioning

confidence: 99%

miRNA-148a inhibits cell growth of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways

Han

Zhu

et al. 2017

Oncology Reports

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The function of miRNA‑148a in lymphatic metastases of papillary thyroid cancer and its mechanism were tested. In this investigation, miRNA‑148a expression of lymphatic metastases of papillary thyroid cancer patients was inhibited, compared with normal group. We found that miRNA‑148a overexpression was effectively reduced cell cell proliferation and metastases, and induced apoptosis of papillary thyroid cancer in vitro. Overexpression of miRNA‑148a significantly induced Bax protein expression and caspase‑3/9 levels, and suppressed phosphorylation STAT3 (p‑STAT3), PI3K and p‑Akt protein expression of papillary thyroid cancer in vitro. Next, si‑STAT3, could inhibit p‑STAT3 protein expression, reducing cell-cell proliferation and metastases, and inducing apoptosis of papillary thyroid cancer following miRNA‑148a overexpression. Then, the PI3K inhibitor was able to inhibit PI3K and p‑Akt protein expression, reduced cell cell proliferation and metastases, and induced apoptosis of papillary thyroid cancer following miRNA‑148a overexpression. Taken together, our results suggest that miRNA‑148a inhibits lymphatic metastases of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways.

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“…It has been identified that miR-148a serves important functions in various types of cancer (35,36). Our previous study demonstrated that miR-148a exerted metastasis-suppressive effects in NSCLC, suppressing NSCLC invasion and metastasis in vitro and in vivo (19).…”

Section: Discussionmentioning

confidence: 98%

Quantitative proteomic analysis of the miR‑148a‑associated mechanisms of metastasis in non‑small cell lung cancer

Chu

Lin

et al. 2018

Oncol Lett

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MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression and protein synthesis. Our previous study demonstrated that miR-148a suppressed the metastasis of non-small cell lung cancer (NSCLC) and. However, the modulatory mechanism of this effect remains unclear. In the present study, quantitative proteomic technology was used to study the protein expression profile of SPC-A-1 cells subsequent to the downregulation of miR-148a expression, in order to elucidate the molecular mechanism of the suppression of NSCLC metastasis by miR-148a. The differentially expressed proteins identified were analyzed using bioinformatics tools, including the Database for Annotation, Visualization and Integrated Discovery and the Search Tool for the Retrieval of Interacting Genes/proteins. In two experiments, 4,048 and 4,083 proteins were identified, and 4,014 and 4,039 proteins were quantified, respectively. In total, 44 proteins were upregulated and 40 proteins were downregulated. This was verified at the protein and mRNA levels by western blotting and reverse transcription-quantitative polymerase chain reaction, respectively. Bioinformatics analysis was used to identify potential interactions and signaling networks for the differentially expressed proteins. This may have provided an appropriate perspective for the comprehensive analysis of the modulatory mechanism underlying the metastasis-suppressive effects of miR-148a in NSCLC. In conclusion, quantitative proteomic technology revealed that miR-148a may regulate a panel of tumor-associated proteins to suppress metastasis in NSCLC.

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Increased expression of microRNA-148a in osteosarcoma promotes cancer cell growth by targeting PTEN

Cited by 30 publications

References 25 publications

miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

miRNA-148a inhibits cell growth of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways

Quantitative proteomic analysis of the miR‑148a‑associated mechanisms of metastasis in non‑small cell lung cancer

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