<scp>ATM</scp>/miR‐34a‐5p axis regulates a p21‐dependent senescence‐apoptosis switch in non‐small cell lung cancer: a Boolean model of G1/S checkpoint regulation

Gupta, Shantanu; Silveira, Daner A.; Mombach, José C. M.

doi:10.1002/1873-3468.13615

Cited by 32 publications

(38 citation statements)

References 88 publications

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“…30 Overexpression of P21 can cause multiple cells to stay in the G1 phase of the cell cycle, leading to apoptosis. 31,32 Related research reported that overexpression of RUNX3 could activate P21 expression. 33 The Figure 8 Relative protein expression in different experimental groups as assessed by immunohistochemistry (×400 magnification) (A) RUNX3 protein expression ***: P<0.001, compared with Vector group; ## P<0.01, compared with MT1JP group (B) Bim protein expression ***P<0.001, compared with Vector group; ## P<0.01, compared with MT1JP group.…”

Section: Discussionmentioning

confidence: 99%

<p>lncRNA MT1JP Suppresses Biological Activities of Breast Cancer Cells in vitro and in vivo by Regulating the miRNA-214/RUNX3 Axis</p>

Ouyang

Cui

Yang

et al. 2020

OTT

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Introduction: The purpose of our research was to evaluate MT1JP in breast cancer. Material and Methods: For clinical purpose, tissues were collected, and a correlation analysis ofMT1JP and miRNA-214 gene expressions was conducted. Using an in vitro study, MDA-MB-231 and MCF-7 cell lines were used as research objects in our research. Colony, flow cytometry, TUNEL, transwell, adhesion and wound healing assay were used to discuss the biological activities of the cells. In an in vivo study, tumor weight and volume were measured, and cell apoptosis was measured by TUNEL assay. The relative mechanism's proteins were evaluated by Western blotting or immunohistochemistry assay. Results: Compared with adjacent tissues, MT1JP and miRNA-214 gene expressions were significantly different (P<0.001, respectively). By in vitro and in vivo studies, the biological activities of the cells were significantly decreased in MDA-MB-231 and MCF-7 cell lines with MT1JP overexpression. The relative mechanism was correlated with miRNA-214/ RUNX3 axis. Conclusion: The overexpression of MT1JP suppresses the biological activities of breast cancer cells by regulation miRNA-214/RUNX3 axis in vitro and vivo study.

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Section: Discussionmentioning

confidence: 99%

<p>lncRNA MT1JP Suppresses Biological Activities of Breast Cancer Cells in vitro and in vivo by Regulating the miRNA-214/RUNX3 Axis</p>

Ouyang

Cui

Yang

et al. 2020

OTT

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“…Hsa-miR-34a-5p is highly expressed in tumor tissues and is closely related to the survival rate [33]. Hsa-miR-34a-5p also acts on the cell cycle and induces apoptosis when it is knocked out [34]. We found that resveratrol reduced the expression of hsa-miR-34a-5p, which helped improve patient survival.…”

Section: Discussionmentioning

confidence: 66%

Integrative investigation of the TF–miRNA coregulatory network involved in the inhibition of breast cancer cell proliferation by resveratrol

Zhou

Zhang

et al. 2021

FEBS Open Bio

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Resveratrol is a polyphenol with antiaging and anticancer effects. Most previous studies used a single analysis to determine the key functions of resveratrol in inhibiting cancer progression. However, most of the signal transmission pathways in biological processes are multilevel. We used bioinformatics to elucidate the mechanism of resveratrol inhibition of breast cancer development. The mRNA expression profile of GSE25412 from the National Center for Biotechnology Information (NCBI) and the microRNA (miRNA) expression profile of PubMed identifier (PMID) 26890143 were integrated. De novo motifs were used to obtain predicted transcription factor (TF) motifs for differentially expressed genes. The regulatory effect of resveratrol on key nodes in the comprehensive analysis results was verified. The TF-miRNA-mRNA interaction network based on the STITCH and miRDB databases showed that resveratrol exerted a dual inhibitory effect by activating inhibitory TFs to block the cell cycle and inhibit miRNAs from upregulating apoptosis. However, these two processes did not work completely independently. TP53 is the dominant hub gene associated with the cell cycle and apoptosis throughout the TF-miRNA network. Kaplan-Meier plotter analysis found that resveratrol-induced expression changes in key RNAs, such as E2F2, JUN, FOS, BRCA1, CDK1, CDKN1A, TNF, and hsa-miR-34a-5p, significantly improved the prognosis of breast cancer patients, which was further verified using real-time quantitative PCR (qPCR) and western blotting. This study constructed a TF-miRNA regulatory network with TP53 and E2F as the main central genes to elucidate the molecular mechanism of resveratrol in the treatment of breast cancer.

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“…It is shown that miR-34a-5p serves as an exosomal transfer RNA and the inhibition of miR-34a-5p mitigated the prosenescent effect in cardiomyocytes and subsequently alleviated the irreversible cell cycle arrest (Xia et al, 2020). miR-34a-5p is also found involved in regulating the switch between senescence and apoptosis in non-small cell lung cancer (Gupta et al, 2020). Herein, we have presented that the inhibition of miR-34a-5p significantly decreases the senescence of HNPCs.…”

Section: Discussionmentioning

confidence: 87%

N6-Methyladenosine Induced miR-34a-5p Promotes TNF-α-Induced Nucleus Pulposus Cell Senescence by Targeting SIRT1

Zhu

Sun

Zhu

et al. 2021

Front. Cell Dev. Biol.

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Low back pain is tightly associated with intervertebral disc degeneration (IVDD) and aberrant nucleus pulposus (NP) is a critical cause. miRNAs N6-methyladenosine (m6A) modification accounts for the TNF-α-induced senescence of NP cells. The aim of this study was to investigate whether m6A modification regulates TNF-α-mediated cell viability, cell cycle arrest, and cell senescence and how it works. The results showed that METTL14 expression positively correlated with m6A and TNF-α expression in HNPCs. The knockdown of METTL14 led to the inhibition of the TNF-α-induced cell senescence. METTL14 overexpression promoted cell senescence. METTL14 regulated the m6A modification of miR-34a-5p and interacted with DGCR8 to process miR-34a-5p. The miR-34a-5p inhibitor inhibited the cell cycle senescence of HNPCs. miR-34a-5p was predicted to interact with the SIRT1 mRNA. SIRT1 overexpression counteracted the miR-34a-5p-promoted cell senescence. METTL14 participates in the TNF-α-induced m6A modification of miR-34a-5p to promote cell senescence in HNPCs and NP cells of IVDD patients. Downregulation of either METTL14 expression or miR-34a-5p leads to the inhibition of cell cycle arrest and senescence. SIRT1 mRNA is an effective binding target of miR-34a-5p, and SIRT1 overexpression mitigates the cell cycle arrest and senescence caused by miR-34a-5p.

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ATM/miR‐34a‐5p axis regulates a p21‐dependent senescence‐apoptosis switch in non‐small cell lung cancer: a Boolean model of G1/S checkpoint regulation

Cited by 32 publications

References 88 publications

<p>lncRNA MT1JP Suppresses Biological Activities of Breast Cancer Cells in vitro and in vivo by Regulating the miRNA-214/RUNX3 Axis</p>

<p>lncRNA MT1JP Suppresses Biological Activities of Breast Cancer Cells in vitro and in vivo by Regulating the miRNA-214/RUNX3 Axis</p>

Integrative investigation of the TF–miRNA coregulatory network involved in the inhibition of breast cancer cell proliferation by resveratrol

N6-Methyladenosine Induced miR-34a-5p Promotes TNF-α-Induced Nucleus Pulposus Cell Senescence by Targeting SIRT1

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