microRNA-199a-3p inhibits hepatic apoptosis and hepatocarcinogenesis by targeting PDCD4

Li, Zhenyang; Zhou, Ye; Zhang, Liyuan; Jia, Kaiwei; Wang, Suyuan; Wang, Mu; Li, Nan; Yu, Yizhi; Cao, Xuetao; Hou, Jin

doi:10.1038/s41389-020-00282-y

Cited by 29 publications

(27 citation statements)

References 48 publications

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“…Total RNA was extracted from human cell lines using RNAiso Plus reagent (Takara, Dalian, China) following the standard protocol. Real-time quantitative RT-PCR (qRT-PCR) analysis was performed using LightCycler 2.0 (Roche, Switzerland) and SYBR RT-PCR kit (Takara) as previously described [ 32 , 33 ]. For gene expression analysis, qPCR primers were human ISG15 (forward: 5’- CGC AGA TCA CCC AGA AGA TCG -3’, reverse: 5’- TTC GTC GCA TTT GTC CAC CA -3’); human long ACE2 (forward: 5’- CAA GAG CAA ACG GTT GAA CAC -3’, reverse: 5’- AGA CTA CAA TGA GAG GCT CTG GG -3’); human dACE2 (forward: 5’- GTG AGA GCC TTA GGT TGG ATT C -3’, reverse: 5’- TAA GGA TCC TCC CTC CTT TGT -3’); human total ACE2 (forward: 5’- TGG GAC TCT GCC ATT TAC TTA C -3’, reverse: 5’- CCC AAC TAT CTC TCG CTT CAT C-3’); internal control human β-actin (forward: 5’-GGC GGC ACC ACC ATG TAC CCT-3’, reverse: 5’-AGG GGC CGG ACT CGT CAT ACT-3’).…”

Section: Methodsmentioning

confidence: 99%

SARS-CoV-2 Spike protein enhances ACE2 expression via facilitating Interferon effects in bronchial epithelium

Zhou

Wang

et al. 2021

Immunology Letters

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Objective In this study, we focused on the interaction between SARS-CoV-2 and host Type I Interferon (IFN) response, so as to identify whether IFN effects could be influenced by the products of SARS-CoV-2. Methods All the structural and non-structural proteins of SARS-CoV-2 were transfected and overexpressed in the bronchial epithelial cell line BEAS-2B respectively, and typical antiviral IFN-stimulated gene (ISG) ISG15 expression was detected by qRT-PCR. RNA-seq based transcriptome analysis was performed between control and Spike (S) protein-overexpressed BEAS-2B cells. The expression of ACE2 and IFN effector JAK-STAT signaling activation were detected in control and S protein-overexpressed BEAS-2B cells by qRT-PCR or/and Western blot respectively. The interaction between S protein with STAT1 and STAT2, and the association between JAK1 with downstream STAT1 and STAT2 were measured in BEAS-2B cells by co-immunoprecipitation (co-IP). Results S protein could activate IFN effects and downstream ISGs expression. By transcriptome analysis, overexpression of S protein induced a set of genes expression, including series of ISGs and the SARS-CoV-2 receptor ACE2. Mechanistically, S protein enhanced the association between the upstream JAK1 and downstream STAT1 and STAT2, so as to promote STAT1 and STAT2 phosphorylation and ACE2 expression. Conclusion SARS-CoV-2 S protein enhances ACE2 expression via facilitating IFN effects, which may help its infection.

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Section: Methodsmentioning

confidence: 99%

SARS-CoV-2 Spike protein enhances ACE2 expression via facilitating Interferon effects in bronchial epithelium

Zhou

Wang

et al. 2021

Immunology Letters

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“…MiR-199a-3p, same as other microRNAs, engages a broad series of mRNA targets, including numerous survival factors and cell cycle regulatory proteins to take effects [ 36 , 37 ]. Thus, the potential promotion of the regenerative response by the miR-199a-3p involves the actions of protein targets that participate in cellular senescence [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA therapy confers anti-senescent effects on doxorubicin-related cardiotoxicity by intracellular and paracrine signaling

Xia

Chang

et al. 2021

Aging

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Doxorubicin (Dox), an important anthracycline, is a potent anticancer agent that is used for treating solid tumors and hematologic malignancies. However, its clinical use is hampered by cardiac cardiotoxicity. This study aimed to investigate the cardioprotective potential of miR-199a-3p. Continuous Dox treatment not only markedly induced cardiomyocyte senescence but also resulted in a growing number of senescence-associated secretory phenotype (SASP) cardiomyocytes, frequently leading to heart senescence. This study showed that miR-199a-3p was downregulated in cardiomyocytes when exposed to Dox. The cardiac-specific overexpression of miR-199a-3p promoted cell cycle re-entry and cell proliferation, resulting in relief from cardiac senescence. Also, the elevation of miR-199a-3p inhibited the generation of SASP, thus, hampering the spread of senescence. In cardiomyocytes, the modulation of miR-199a-3p changed the levels of senescence-related protein GATA4. The ectopic expression of GATA4 blunted the anti-senescence effect of miR-199a-3p. Together, the data supported a role for miR-199a-3p during Dox cardiotoxicity. The elevation of miR-199a-3p might provide a dual therapeutic advantage in Dox cardiotoxicity therapy by simultaneously preventing cardiac senescence and reducing the spread of senescence.

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“…For example, miR-342-3p inhibits the initiation and progression of hepatocellular carcinoma by regulating MTC1 [19]. miR-199a-3p inhibits the oncogenesis of hepatocellular carcinoma and hepatic apoptosis via targeting programmed cell death 4 [20]. As a newly identified miRNA, miR-100 also regulated tumor initiation and progression.…”

Section: Discussionmentioning

confidence: 99%

miR-100 Suppresses the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma Cells via Targeting CXCR7

Shu

Shi

et al. 2021

Journal of Immunology Research

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This study is to elucidate the functions of miR-100 in hepatocellular carcinoma progression and to explore the underlying mechanisms. Expression levels of miR-100 in normal-cancer hepatocellular carcinoma tissues were measured using quantitative real-time PCR (qRT-PCR). The invasive and proliferative abilities of hepatocellular carcinoma cell lines transfected with mimic-NC or mimic-miR-100 were measured using transwell, CCK-8, and colony formation assays. The binding sites between CXCR7 and miR-100 were determined using luciferase reporter assays. The correlation of CXCR7 and miR-100 in hepatocellular carcinoma progression was further confirmed by cotransfection assays. Our results showed that miR-100 was significantly lower expressed in hepatocellular carcinoma tissues and negatively associated with CXCR7 expression. Cell functional assays’ results found that upregulation of miR-100 inhibited the proliferative, invasive, and migrative abilities in hepatocellular carcinoma cells. Luciferase reporter assay suggested that CXCR7 mRNA and miR-100 bound one another. Increasing CXCR7 expression reversed the inhibitive effects of upregulated miR-100 in hepatocellular carcinoma cells. Further study showed that miR-100/CXCR7 played a role in hepatocellular carcinoma progression by regulating metalloproteinase-2 (MMP2) and vascular endothelial growth factor (VEGF). Conclusively, miR-100 exerts antitumor effects on hepatocellular carcinoma. Overexpression of miR-100 attenuates the invasive and proliferative abilities of hepatocellular carcinoma cells by targeting CXCR7.

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microRNA-199a-3p inhibits hepatic apoptosis and hepatocarcinogenesis by targeting PDCD4

Cited by 29 publications

References 48 publications

SARS-CoV-2 Spike protein enhances ACE2 expression via facilitating Interferon effects in bronchial epithelium

SARS-CoV-2 Spike protein enhances ACE2 expression via facilitating Interferon effects in bronchial epithelium

MicroRNA therapy confers anti-senescent effects on doxorubicin-related cardiotoxicity by intracellular and paracrine signaling

miR-100 Suppresses the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma Cells via Targeting CXCR7

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