Micro<scp>RNA</scp>‐155‐5p promotes hepatocellular carcinoma progression by suppressing <scp>PTEN</scp> through the <scp>PI</scp>3K/Akt pathway

Fu, Xiao; Wen, Hongqing; Li, Jing; Yang, Yujuan; Wang, Wenjuan; Liu, Xuan; Kang, Nan; Yao, Yu; Tian, Tao

doi:10.1111/cas.13177

Cited by 133 publications

(111 citation statements)

References 32 publications

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“…These factors are related to certain cellular biological processes, such as cell proliferation, migration, apoptosis, and angiogenesis. For example, PTEN is well known as a key factor in the PI3 K/Akt signaling and acts as a suppessor gene of hepatocellular carcinoma . To our surprise, La and La‐related protein are closely connected to liver cancer .…”

Section: Discussionmentioning

confidence: 89%

Alteration of microRNA profiles by a novel inhibitor of human La protein in HBV‐transformed human hepatoma cells

Pan

Tong

Tang

2017

Journal of Medical Virology

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A pyrazolopyridine HBSC11 was previously identified as a novel inhibitor of human La protein with anti‐hepatitis B virus (HBV) activity. However, the underlying mechanism(s) of HBV inhibition by HBSC11 remains unclear. This study aimed to examine the regulation of microRNA (miRNA) by HBSC11 in HBV‐transformed human hepatoma HepG2.2.15 cells using microarray and quantitative real‐time PCR. Target genes of the differentially expressed miRNAs were predicted and subjected to bioinformatics analysis. Results showed that HBSC11 significantly upregulated the expression of miR‐3912‐5p, miR‐6793‐5p, and miR‐7159‐5p in HepG2.2.15 cells. Target genes of the three miRNAs were mainly involved in the regulation of nucleic acid‐templated transcription, negative regulation of gene expression, nucleic acid binding transcription factor activity and regulation of phosphorylation. In addition, target genes were enriched in certain regulatory pathways related to HBV infection and HBV‐associated disease progression, such as the transforming growth factor (TGF)‐β, Wnt, and p53 signaling. Our study demonstrates the involvement of miR‐3912‐5p, miR‐6793‐5p, and miR‐7159‐5p and the potential modulation of specific pathways (TGF‐β, Wnt, and p53 signaling) in HBSC11‐mediated inhibition of HBV replication. This study provides insight into the molecular mechanism of the action of HBSC11 against HBV infection and will support the development of antiviral drugs targeting La protein.

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Section: Discussionmentioning

confidence: 89%

Alteration of microRNA profiles by a novel inhibitor of human La protein in HBV‐transformed human hepatoma cells

Pan

Tong

Tang

2017

Journal of Medical Virology

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“…22,25 As shown in Figure 4A,B, we found that overexpression of miR-623 did not affect the total level of Akt and mammalian target of rapamycin (mTOR), whereas phosphorylated form p-Akt and p-mTOR was significantly inhibited in HCC cells. * P < .05 compared with negative control (NC).…”

Section: F I G U R E 3 Upregulation Of Mir-623 Induces Apoptosis Of Hmentioning

confidence: 88%

“…[22][23][24][25] Inhibiting these signaling pathways is considered to be an effective method for cancer therapy. [22][23][24][25] Inhibiting these signaling pathways is considered to be an effective method for cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‐623 suppresses progression of hepatocellular carcinoma via regulating the PI3K/Akt signaling pathway by targeting XRCC5

Ren

Jiang

et al. 2019

J of Cellular Biochemistry

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It has been reported that miR‐623 is deregulated in lung adenocarcinoma and inhibits tumor growth and invasion. However, it is unclear whether miR‐623 has a role in the progression of hepatocellular carcinoma (HCC). Herein, we found that miR‐623 was significantly downregulated in HCC, and that its expression was related to poor clinical outcomes of patients with HCC. Upregulation of miR‐623 decreased cell proliferation, viability, migration, and invasion and further promoted apoptosis in 7721, Huh7, and Bel‐7402 cells. Moreover, we also observed that miR‐623 regulated the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt), Wnt/β‐catenin, and extracellular regulated protein kinases/c‐Jun N‐terminal kinase (ERK/JNK) signaling pathways as well as the expression level of related proteins. Further, X‐ray repair cross complementing 5 (XRCC5) was a direct target for miR‐623, and the suppression of PI3K/Akt, Wnt/β‐catenin, and ERK/JNK signaling pathways and cell proliferation and invasion abilities caused by miR‐623 in HCC cells was significantly reversed by the upregulation of XRCC5. Collectively, our data suggested that miR‐623 suppressed the progression of HCC by regulating the PI3K/Akt, Wnt/β‐catenin, and ERK/JNK pathways by targeting XRCC5 in HCC in vitro, indicating that miR‐623 may be a target for the therapy of HCC.

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“…AKT is a key regulatory factor of cell proliferation (21). In the present study, the expression of AKT was knocked down in a HaCaT cell model via siRNA silencing.…”

Section: The Function Of Akt In Hacat Cell Proliferation and Mitosismentioning

confidence: 88%

MicroRNA‑520a suppresses the proliferation and mitosis of HaCaT cells by inactivating protein kinase B

et al. 2017

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Abstract. Psoriasis is a chronic inflammatory disease of the skin for which an effective treatment strategy remains to be developed. Characteristics of psoriasis include an altered differentiation of keratinocytes and hyperplasia of the skin. The present study aimed to investigate the role served by miR-520a in psoriasis. The results demonstrated that miR-520a inhibited the proliferation of HaCaT cells. miR-520a directly regulated the mRNA and protein expression of its target gene, protein kinase B (AKT). The siRNA silencing of AKT expression in these cells was also evaluated. miRNA-520a repressed the proliferation and mitotic entry of HaCaT cells, and promoted cell apoptosis. AKT silencing suppressed the proliferation of HaCaT cells. These results suggest that miRNA-520a regulates the survival of HaCaT cells by inhibiting AKT expression. miRNA-520a and AKT may therefore be novel targets for the treatment of patients with psoriasis.

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MicroRNA‐155‐5p promotes hepatocellular carcinoma progression by suppressing PTEN through the PI3K/Akt pathway

Cited by 133 publications

References 32 publications

Alteration of microRNA profiles by a novel inhibitor of human La protein in HBV‐transformed human hepatoma cells

Alteration of microRNA profiles by a novel inhibitor of human La protein in HBV‐transformed human hepatoma cells

Overexpression of miR‐623 suppresses progression of hepatocellular carcinoma via regulating the PI3K/Akt signaling pathway by targeting XRCC5

MicroRNA‑520a suppresses the proliferation and mitosis of HaCaT cells by inactivating protein kinase B

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