miR‑186 functions as a tumor suppressor in osteosarcoma cells by suppressing the malignant phenotype and aerobic glycolysis

Xiao, Qianren; Wei, Zhihui; Li, Yunyun; Zhou, Xin; Chen, Jiajun; Wang, Tengyu; Shao, Gaohai; Zhang, Minghua; Zhang, Zhongzu

doi:10.3892/or.2018.6394

Cited by 24 publications

(26 citation statements)

References 17 publications

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“…To further explore the mechanism of upstream signaling of Shp2, we predicted the targeting relationship between miR-186 and Shp2 through the website. It's reported that miR-186 inhibits the development of non-small lung cancer, colon cancer, cervical cancer and gastric cancer [27][28][29][30]. In our study, dual luciferase reporter assay confirmed that miR-186 negatively regulates Shp2 gene.…”

Section: Discussionsupporting

confidence: 78%

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Yan

Zheng

et al. 2020

Preprint

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Background The study aimed to investigate the effect and mechanism of miR-186, which targets protein tyrosine phosphatase (Shp2) PI3K/Akt/mTOR signaling pathway, on the biological characteristics of lung adenocarcinoma cells. Methods In this experimental study, Human lung adenocarcinoma cell line SPC-A-1 was grouped as Blank group, negative control (NC) group, miR-186 mimic group, miR-186 inhibitor group, si-Shp2 group and miR-186 inhibitor+si-Shp2 group. Results The results showed that miR-186 can target and down-regulate the expression of Shp2 gene. Compared with the Blank group, levels of Shp2, N-cadherin and Bcl-2 and level of PI3K/p-PI3K, Akt/P-Akt, mTOR/p-mTOR as well as cell proliferation, migration and invasion ability and the proportion of cells in S phase significantly decreased in the miR-186 mimic group and the si-Shp2 group, while the levels of E-cadherin and Bax as well as the proportion of cells in G1 phase and cell gene and mediates apoptosis rate increased significantly (all P < 0.05). Compared with the miR-186 inhibitor group, the miR-186 inhibitor + si-Shp2 group showed similar trend in all parameters with the comparison above (all P < 0.05). Conclusions The overexpression of miR-186 can down-regulate Shp2 gene expression, further inhibit the proliferation, invasion and migration and promote apoptosis of lung adenocarcinoma cells by inhibiting the activation of PI3K/Akt/mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 78%

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Yan

Zheng

et al. 2020

Preprint

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“…Osteosarcoma (OS) is a primary malignant tumor of the skeleton characterized by the direct formation of immature bone or osteoid tissue in the tumor cells. 1 More rarely, OS may arise in the soft tissue. About 75% of cases, patients with OS are between 15 and 25 years of age.…”

Section: Introductionmentioning

confidence: 99%

Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A

Jin

Chen

Líu

et al. 2019

Clinical Laboratory Analysis

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ObjectiveTo screen the gene related to osteosarcoma (OS) metastasis and the molecular mechanism.MethodsGEO database and R2 chip analysis platform were used to screen genes related to OS metastasis. UCSC gene browser was used to find the transcription factor (TF) of CLEC5A. The mRNA level and protein expression of CLEC5A in OS tissues and normal tissues were determined by RT‐PCR and Western blotting, respectively. OS cell lines MG‐63 were transfected with CEBPB recombinant plasmid. After transfection, the expression of CLEC5A in MG‐63 cells was determined and the cell proliferation situation was determined by clone formation assay.ResultsThree genes CLEC5A, ALOX5AP, and RNASE3 were obtained, and CLEC5A has the highest correlation with OS. CLEC5A has screened the gene related to OS metastasis, and CEBPB can be taken as TF regulating downstream gene CLEC5A. CEBPB can regulate the downstream CLEC5A as transcription factor. The relative mRNA level and protein expression of CLEC5A in OS tissues were significantly higher than those in normal tissues. CLEC5A can prevent OS metastasis. Transfection of CEBPB increased the expression of CLEC5A in MG‐63 cells and also inhibited the proliferation of OS.ConclusionCEBPB can inhibit the proliferation of OS cells via regulating the expression of CLEC5A.

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“…In agreement, miR-323a-3p results significantly downregulated in OS tissues and cell lines, while its overexpression reduces cell viability [150]. In addition, a different miRNA, namely miR-186, which decreases indirectly lactate levels through direct inhibition of HIF-1α and glycolysis, functions as a tumor suppressor of both HOS and U2 OS cell lines, inhibiting tumor cell proliferation and invasion [151].…”

Section: Lactate and Sarcomasmentioning

confidence: 73%

Lactate in Sarcoma Microenvironment: Much More than just a Waste Product

Taddei

Pietrovito

Leo

et al. 2020

Cells

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Sarcomas are rare and heterogeneous malignant tumors relatively resistant to radio- and chemotherapy. Sarcoma progression is deeply dependent on environmental conditions that sustain both cancer growth and invasive abilities. Sarcoma microenvironment is composed of different stromal cell types and extracellular proteins. In this context, cancer cells may cooperate or compete with stromal cells for metabolic nutrients to sustain their survival and to adapt to environmental changes. The strict interplay between stromal and sarcoma cells deeply affects the extracellular metabolic milieu, thus altering the behavior of both cancer cells and other non-tumor cells, including immune cells. Cancer cells are typically dependent on glucose fermentation for growth and lactate is one of the most heavily increased metabolites in the tumor bulk. Currently, lactate is no longer considered a waste product of the Warburg metabolism, but novel signaling molecules able to regulate the behavior of tumor cells, tumor-stroma interactions and the immune response. In this review, we illustrate the role of lactate in the strong acidity microenvironment of sarcoma. Really, in the biological context of sarcoma, where novel targeted therapies are needed to improve patient outcomes in combination with current therapies or as an alternative treatment, lactate targeting could be a promising approach to future clinical trials.

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miR‑186 functions as a tumor suppressor in osteosarcoma cells by suppressing the malignant phenotype and aerobic glycolysis

Cited by 24 publications

References 17 publications

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A

Lactate in Sarcoma Microenvironment: Much More than just a Waste Product

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