Let-7a inhibits migration, invasion and tumor growth by targeting AKT2 in papillary thyroid carcinoma

Zhou, Bin; Shan, Hailin; Su, Ying; Xia, Kai; Zou, Runlong; Shao, Qing

doi:10.18632/oncotarget.19261

Cited by 21 publications

(27 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miRNA is a class of endogenous non‐coding small RNA molecule. It generally targets one or more mRNAs and binds with its 3′‐untranslated region (3′‐UTR) . Thus, it can inhibit or degrade the target miRNA at translation level and negatively regulate target gene expression .…”

Section: Introductionmentioning

confidence: 99%

miR‐98‐5p promotes apoptosis and inhibits migration and cell growth in papillary thyroid carcinoma through Bax/Caspase‐3 by HMGA2

Qiu

Xie

Jiang

et al. 2019

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background The aims of this study were to investigate the function and mechanism of miRNA‐98‐5p in papillary thyroid carcinoma. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to measure the expression of miRNA‐98‐5p in papillary thyroid carcinoma. Western blotting and caspase‐3/9 activity levels, flow cytometric analysis, cell migration assays, DAPI assay, cell proliferation assay, and LDH activity levels were used in this study. Results In patient with papillary thyroid carcinoma, miRNA‐98‐5p was reduced, and HMGA2 was increased. Downregulation of miRNA‐98‐5p promoted the cell growth, inhibited apoptosis, and induced HMGA2 protein expression in papillary thyroid carcinoma cell via activation of HMGA2. Overexpression of miRNA‐98‐5p inhibited the cell growth, induced apoptosis, and suppressed HMGA2 protein expression in papillary thyroid carcinoma cell through the suppression of HMGA2. Si‐HMGA2 inhibited the effects of anti‐miRNA‐98‐5p on cell growth of papillary thyroid carcinoma. Conclusion Therefore, these results suggested the regulation of HMGA2 suppresses proliferation of papillary thyroid carcinoma through miRNA‐98‐5p.

show abstract

Section: Introductionmentioning

confidence: 99%

miR‐98‐5p promotes apoptosis and inhibits migration and cell growth in papillary thyroid carcinoma through Bax/Caspase‐3 by HMGA2

Qiu

Xie

Jiang

et al. 2019

Clinical Laboratory Analysis

View full text Add to dashboard Cite

show abstract

“…Selective cleavage after PKM transcription was regulated by heterogeneous nuclear ribonucleoprotein (hnRNP)-A1, hnRNP-A2, and polypyrimidine tract binding (PTB). [19][20][21] In this study, we explored the role of let-7a-5p and PKM2 in the aerobic glycolysis of breast cancer cells. [13][14][15] Some of the related studies of Stat3 oncogene have laid a foundation for the interpretation and treatment of breast cancer formation mechanism.…”

mentioning

confidence: 99%

PKM2 promotes glucose metabolism through a let‐7a‐5p/Stat3/hnRNP‐A1 regulatory feedback loop in breast cancer cells

Yao

Yuan

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Tumor cells metabolize more glucose to lactate in aerobic or hypoxic conditions than normal cells. Pyruvate kinase isoenzyme type M2 (PKM2) is crucial for tumor cell aerobic glycolysis. We established a role for let‐7a‐5p/Stat3/hnRNP‐A1/PKM2 signaling in breast cancer cell glucose metabolism. PKM2 depletion via small interfering RNA (siRNA) inhibits cell proliferation and aerobic glycolysis in breast cancer cells. Signal transducer and activator of transcription 3 (Stat3) promotes upregulation of heterogeneous nuclear ribonucleoprotein (hnRNP)‐A1 expression, hnRNP‐A1 binding to pyruvate kinase isoenzyme (PKM) pre messenger RNA, and the subsequent formation of PKM2. This pathway is downregulated by the microRNA let‐7a‐5p, which functionally targets Stat3, whereas hnRNP‐A1 blocks the biogenesis of let‐7a‐5p to counteract its ability to downregulate the Stat3/hnRNP‐A1/PKM2 signaling pathway. The downregulation of Stat3/hnRNP‐A1/PKM2 by let‐7a‐5p is verified using a breast cancer. These results suggest that let‐7a‐5p, Stat3, and hnRNP‐A1 form a feedback loop, thereby regulating PKM2 expression to modulate glucose metabolism of breast cancer cells. These findings elucidate a new pathway mediating aerobic glycolysis in breast cancers and provide an attractive potential target for breast cancer therapeutic intervention.

show abstract

“…38 miR Let-7a-5p expression was also suppressed 9.5-fold after LCHS/ CS compared with LCHS/CSþBB and naïve animals and its expression has been studied in thyroid carcinoma and cellular proliferation in relation to the Akt pathway. 39 The phosphoinositide 3-kinase-Akt signaling pathway plays an important role in erythropoiesis and can downregulate apoptosis of erythroblasts. 40 MicroRNA-146a was also suppressed 15-fold in the LCHS/CS group compared with LCHS/CSþBB and naïve rodents.…”

Section: Discussionmentioning

confidence: 99%

Effect of Beta-Blockade on the Expression of Regulatory MicroRNA after Severe Trauma and Chronic Stress

Miller

Loftus

Kannan

et al. 2020

Journal of the American College of Surgeons

View full text Add to dashboard Cite

BACKGROUND: Beta-blockade administration after lung contusion, hemorrhagic shock, and chronic stress has been shown to improve bone marrow function, decrease hypercatecholaminemia, and reduce inflammation. MicroRNAs (miR) are critical biologic regulators that can downregulate gene expression by causing messenger RNA degradation or inhibition of translation. This study sought to expand our understanding of the molecular mechanisms underlying the reduced inflammatory response after the administration of beta-blockade (BB) in our rodent trauma model. STUDY DESIGN: Male Sprague-Dawley rats aged 8 to 9 weeks were randomized to lung contusion, hemorrhagic shock with daily restraint stress (LCHS/CS) or LCHS/CS plus propranolol (LCHS/ CSþBB). Restraint stress occurred 2 hours daily after LCHS. Propranolol (10 mg/kg) was given daily until day 7. Total RNA and miR were isolated from bone marrow and genomewide miR expression patterns were assayed. Bone marrow cytokine expression was determined with quantitative polymerase chain reaction. RESULTS: LCHS/CS led to significantly increased bone marrow expression of interleukin (IL) 1b, tumor necrosis factor-a, IL-6, nitric oxide, and plasma C-reactive protein. There were marked differences in expression of 45 miRs in the LCHS/CSþBB group compared with the LCHS/CS group when using a p value <0.001. Rno-miR-27a and miR-25 were upregulated 7-to 8-fold in the rodents who underwent LCHS/CSþBB compared with LCHS/CS alone, and this correlated with reduced bone marrow expression of IL-1b, tumor necrosis factor-a, IL-6, nitric oxide, and reduced plasma C-reactive protein in the LCHS/CSþBB group. CONCLUSIONS: The genomic and miR expression patterns in bone marrow after LCHS/CS differed significantly compared with rodents that received propranolol after LCHS/CS. The use of BB after severe trauma can help mitigate persistent inflammation by upregulating Rno-miR-27a and miR-25 and reducing inflammatory cytokines in those who remain critically ill.

show abstract

Let-7a inhibits migration, invasion and tumor growth by targeting AKT2 in papillary thyroid carcinoma

Cited by 21 publications

References 28 publications

miR‐98‐5p promotes apoptosis and inhibits migration and cell growth in papillary thyroid carcinoma through Bax/Caspase‐3 by HMGA2

miR‐98‐5p promotes apoptosis and inhibits migration and cell growth in papillary thyroid carcinoma through Bax/Caspase‐3 by HMGA2

PKM2 promotes glucose metabolism through a let‐7a‐5p/Stat3/hnRNP‐A1 regulatory feedback loop in breast cancer cells

Effect of Beta-Blockade on the Expression of Regulatory MicroRNA after Severe Trauma and Chronic Stress

Contact Info

Product

Resources

About