RhoA inhibits apoptosis and increases proliferation of cultured SPCA1 lung cancer cells

Liu, Dabei; Mei, Xingke; Wang, Linlin; Yang, Xueying

doi:10.3892/mmr.2017.6545

Cited by 20 publications

(17 citation statements)

References 22 publications

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“…Next, we explored the probable mechanisms involved in the TNS1-mediated cell growth and metastases. Akt/mTOR and RhoA signaling pathway are both critical in lung cancer development [ 24 , 25 ], which are reported to be regulated by TNS1 [ 26 , 27 ]. The results implied that pcDNA3.1-TNS1 increased p-AKT/AKT ratio and p-mTOR/mTOR ratio.…”

Section: Resultsmentioning

confidence: 99%

miR-152/TNS1 axis inhibits non-small cell lung cancer progression through Akt/mTOR/RhoA pathway

et al. 2021

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Aim: The purpose of the present study was to explore the function and mechanism of tensin 1 (TNS1) in non-small cell lung cancer (NSCLC) progression. Methods: The expression of TNS1 in NSCLC cells and tissues was assessed by RT-PCR and Western blot. Besides, Kaplan–Meier survival analysis was recruited to explore the association between TNS1 and NSCLC. Cell growth was analyzed by MTT and flow cytometry assay, while cell metastasis was determined by wound healing and transwell assays. The targeting relationship between TNS1 and miR-152 was assessed by luciferase activity assays. And Western blot was employed to determine the expression of related proteins of Akt/mTOR/RhoA pathway. Results: TNS1 level was boosted in NSCLC cells and tissues, related to the prognosis of NSCLC patients. Furthermore, it was proved that TNS1 promoted the growth and metastasis of NSCLC cells via Akt/mTOR/RhoA pathway. And miR-152 targeted TNS1 to affect the progression of NSCLC. Conclusion: miR-152/TNS1 axis inhibits the progression of NSCLC by Akt/mTOR/RhoA pathway.

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Section: Resultsmentioning

confidence: 99%

miR-152/TNS1 axis inhibits non-small cell lung cancer progression through Akt/mTOR/RhoA pathway

et al. 2021

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“…Alternatively, increased RhoA signaling could inhibit programmed cell death, thereby increasing the viability of the cells. This protective effect is well characterized [41][42][43]. Mariani et al [16] discovered that migrating glioma cells not only have increased ARHGAP29 expression but also a down-regulation of proliferation-relevant genes.…”

Section: Discussionmentioning

confidence: 93%

Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

Kolb

Hellinger

Kansy

et al. 2020

Cells

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Aggressive and mesenchymal-transformed breast cancer cells show high expression levels of Rho GTPase activating protein 29 (ARHGAP29), a negative regulator of RhoA. ARHGAP29 was the only one of 32 GTPase-activating enzymes whose expression significantly increased after the induction of mesenchymal transformation in breast cancer cells. Therefore, we investigated the influence of ARHGAP29 on the invasiveness of aggressive and mesenchymal-transformed breast cancer cells. After knock-down of ARHGAP29 using siRNA, invasion of HCC1806, MCF-7-EMT, and T-47D-EMT breast cancer cells was significantly reduced. This could be explained by reduced inhibition of RhoA and a consequent increase in stress fiber formation. Proliferation of the breast cancer cell line T-47D-EMT was slightly increased by reduced expression of ARHGAP29, whereas that of HCC1806 and MCF-7-EMT significantly increased. Using interaction analyses we found that AKT1 is a possible interaction partner of ARHGAP29. Therefore, the expression of AKT1 after siRNA knock-down of ARHGAP29 was tested. Reduced ARHGAP29 expression was accompanied by significantly reduced AKT1 expression. However, the ratio of active pAKT1 to total AKT1 remained unchanged or was significantly increased after ARHGAP29 knock-down. Our results show that ARHGAP29 could be an important factor in the invasion of aggressive and mesenchymal-transformed breast cancer cells. Further research is required to fully understand the underlying mechanisms.

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“…A recent study highlighted that RhoA might be important for the proliferation and apoptosis in lung cancer cells. Alterations in caspase-3 may be the underlying molecular mechanisms associated with the effect of RhoA on cell proliferation and apoptosis [71].…”

Section: Discussionmentioning

confidence: 99%

Experimental validation and computational modeling of anti-influenza effects of quercetin-3-O-α-L-rhamnopyranoside from indigenous south African medicinal plant Rapanea melanophloeos

Mehrbod

Ebrahimi

Fotouhi

et al. 2019

BMC Complement Altern Med

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Background: Influenza A virus (IAV) is still a major health threat. The clinical manifestations of this infection are related to immune dysregulation, which causes morbidity and mortality. The usage of traditional medication with immunomodulatory properties against influenza infection has been increased recently. Our previous study showed antiviral activity of quercetin-3-O-α-L-rhamnopyranoside (Q3R) isolated from Rapanea melanophloeos (RM) (L.) Mez (family Myrsinaceae) against H1N1 (A/PR/8/34) infection. This study aimed to confirm the wider range of immunomodulatory effect of Q3R on selective pro-and anti-inflammatory cytokines against IAV in vitro, to evaluate the effect of Q3R on apoptosis pathway in combination with H1N1, also to assess the physical interaction of Q3R with virus glycoproteins and RhoA protein using computational docking. Methods: MDCK cells were exposed to Q3R and 100CCID 50 /100 μl of H1N1 in combined treatments (co-, pre-and post-penetration treatments). The treatments were tested for the cytokines evaluation at RNA and protein levels by qPCR and ELISA, respectively. In another set of treatment, apoptosis was examined by detecting RhoA GTPase protein and caspase-3 activity. Molecular docking was used as a tool for evaluation of the potential anti-influenza activity of Q3R. Results: The expressions of cytokines in both genome and protein levels were significantly affected by Q3R treatment. It was shown that Q3R was much more effective against influenza when it was applied in co-penetration treatment. Q3R in combination with H1N1 increased caspase-3 activity while decreasing RhoA activation. The molecular docking results showed strong binding ability of Q3R with M2 transmembrane, Neuraminidase of 2009 pandemic H1N1, N1 and H1 of PR/8/1934 and Human RhoA proteins, with docking energy of − 10.81, − 10.47, − 9.52, − 9.24 and − 8.78 Kcal/mol, respectively.(Continued on next page)

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RhoA inhibits apoptosis and increases proliferation of cultured SPCA1 lung cancer cells

Cited by 20 publications

References 22 publications

miR-152/TNS1 axis inhibits non-small cell lung cancer progression through Akt/mTOR/RhoA pathway

miR-152/TNS1 axis inhibits non-small cell lung cancer progression through Akt/mTOR/RhoA pathway

Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

Experimental validation and computational modeling of anti-influenza effects of quercetin-3-O-α-L-rhamnopyranoside from indigenous south African medicinal plant Rapanea melanophloeos

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