MiRNA-10a is upregulated in NSCLC and may promote cancer by targeting PTEN

Tao, Yu; Liu, Lei; Li, Jing; Yan, Mingxia; Lin, Hechun; Liu, Ying; Chu, Dandan; Tu, Hong; Gu, Aiqin; Yao, Ming

doi:10.18632/oncotarget.4972

Cited by 117 publications

(89 citation statements)

References 38 publications

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“…McCarroll has reported that loss of PTEN/AKT activity can promote tumorigenesis in NSCLC, which explains the changes in proliferation and cell cycle between the treated and control cells [41]. Additionally, as a downstream molecule of many regulatory factors, such as miRNA-10a, TOPK/PBK, PUMA and others, PTEN/AKT has been shown to influence the drug resistance and prognosis of NSCLC [37, 42-44]. Furthermore, we reduced the expression of PTEN in FAL1 knockdown cells and found that the effect of FAL1 siRNA interference was partially rescued, which demonstrated our assumption of the presence of a FAL1-PTEN/AKT-EMT regulation pathway.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

Pan

Yao

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Recently, long non-coding RNAs (lncRNAs) have been found to have many biological effects in different cancer stages. Several studies have revealed that focally amplified lncRNA on chromosome 1 (FAL1) regulates cancer progression via p21. However, the expression and mechanism of FAL1 in non-small cell lung cancer (NSCLC) still remain unclear. Methods: We detected the FAL1 level in NSCLC tissues and in established cell lines using quantitative real-time PCR and evaluated the clinical significance. FAL1 was silenced or overexpressed using siRNA or lentivirus to study whether FAL1 affected cell proliferation, invasion and migration. Xenograft growth and pulmonary metastasis were observed using nude mouse models. The mechanisms were explored with western blotting and immunohistochemistry. Results: FAL1 was significantly overexpressed in NSCLC compared with adjacent normal tissues, and a high level of FAL1 correlated with poor histological grade, increased lymph node metastasis and advanced TNM stage. Loss- and gain-of-function experiments in vitro verified that knockdown of FAL1 inhibited cell proliferation, invasion, migration and EMT via the PTEN/AKT pathway. Furthermore, an in vivo assay confirmed that overexpression of FAL1 facilitated tumor growth and metastasis. Conclusion: FAL1 may promote tumorigenesis and progression of NSCLC through the PTEN/AKT axis, which could lead to lncRNA-related diagnostics and therapeutics in NSCLC.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

Pan

Yao

Liu

et al. 2017

Cell Physiol Biochem

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“…The target mRNAs of miRNAs are being uncovered, including the verified targets for miR-10a, such as fms-related tyrosine kinase 1,27) cell adhesion molecule L1-like, 28) phosphatase and tensin homolog, 29) and EPH receptor A8 30) in some diseases. More importantly, miR-10a is found to repress TBX5 protein levels by targeting TBX5 3'UTR.…”

Section: Discussionmentioning

confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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SummaryThe mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy. (Int Heart J 2017; 58: 100-106)

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“…Several miRNAs that were downregulated by Gal-9 treatment have been reported to be associated with cancer cell apoptosis. For instance, miR-10a has been reported to be upregulated in several solid tumors including pancreatic cancer (35) and lung cancer (36). miR-10a targets the phosphatase and tensin homolog (PTEN), and miR-10a promotes the migration, invasion, and growth of non-small cell lung cancer by regulating the PTEN/AKT/ERK signaling pathway (36).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, miR-10a has been reported to be upregulated in several solid tumors including pancreatic cancer (35) and lung cancer (36). miR-10a targets the phosphatase and tensin homolog (PTEN), and miR-10a promotes the migration, invasion, and growth of non-small cell lung cancer by regulating the PTEN/AKT/ERK signaling pathway (36). In addition, miR-224 promotes lung cancer cells proliferation and migration by direct targeting of caspase-3 and caspase-7 (37), and downregulation of miR-224 might be associated with inhibition of cancer progression by inducing apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Galectin-9: An anticancer molecule for gallbladder carcinoma

Tadokoro

Morishita

Fujihara

et al. 2016

International Journal of Oncology

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Abstract. Gallbladder cancer (GBC) is the most common and aggressive type of biliary tract cancer. There are various histological types of GBC, and the vast majority of GBC cases are adenocarcinomas. Squamous and adenosquamous carcinomas are rare GBC subtypes that are traditionally considered to be more aggressive and to be associated with a poorer prognosis than adenocarcinoma. Galectin-9 (Gal-9), a tandem-repeattype galectin, has been reported to induce apoptosis-mediated elimination of various cancers, including hepatocellular carcinoma, cholangiocarcinoma, and hematologic malignancies. Therefore, we investigated the antitumor effects of Gal-9 on GBC in vitro and in vivo. In our in vitro experiments, Gal-9 suppressed cell proliferation in various GBC cell lines but not in the OCUG-1 cell line, which represents a poorly differentiated type of adenosquamous carcinoma. Gal-9 induced the apoptosis of Gal-9-sensitive GBC cells by increasing the levels of caspase-cleaved keratin 18 and phosphorylated p53. However, Gal-9 did not affect the expression of various cell cycle-related proteins. In addition, Gal-9 suppressed tumor growth by implanted human GBC cells in a xenograft model. Furthermore, Gal-9 induced the phosphorylation of the Ephrin type-B receptor, and the microRNA (miRNA) expression profile was markedly altered by Gal-9. Based on these results, various miRNAs might contribute to the suppression of tumor growth. Our data reveal that Gal-9 suppresses the growth of GBC, possibly by inducing apoptosis and altering miRNA expression. Thus, Gal-9 might serve as a therapeutic agent for the treatment of GBC.

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MiRNA-10a is upregulated in NSCLC and may promote cancer by targeting PTEN

Cited by 117 publications

References 38 publications

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Galectin-9: An anticancer molecule for gallbladder carcinoma

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