Ad-apoptin inhibits glycolysis, migration and invasion in lung cancer cells targeting AMPK/mTOR signaling pathway

Song, Gaojie; Fang, Jinbo; Shang, Chao; Li, Yiquan; Zhu, Yan; Xiu, Zhiru; Sun, Lili; Jin, Ningyi; Li, Xiao

doi:10.1016/j.yexcr.2021.112926

Cited by 15 publications

(20 citation statements)

References 29 publications

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“…For example, activating AMPK-mTOR-ULK1 reinforced autophagy, apoptosis, and cytotoxicity in human bladder cancer induced by10-hydroxycamptothecin [45]. The AMPK-mTOR axis took part in NSCLC treatment by inhibiting cell proliferation, migration, invasion, and glycolysis and activating oxidative stress, autophagy, and apoptosis [46][47][48][49]. In the present study, RSV activated AMPK and mTOR by phosphorylation.…”

Section: Discussionsupporting

confidence: 50%

Resveratrol Induces Autophagy and Apoptosis in Non-Small-Cell Lung Cancer Cells by Activating the NGFR-AMPK-mTOR Pathway

Fan

Zhang

et al. 2022

Nutrients

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Resveratrol (RSV) has been reported to induce autophagy and apoptosis in non-small-cell lung cancer A549 cells, and the nerve growth factor receptor (NGFR) regulates autophagy and apoptosis in many other cells. However, the effect of NGFR on autophagy and apoptosis induced by RSV in A549 cells remains unclear. Here, we found that RSV reduced the cell survival rate in time- and concentration-dependent manners, activating autophagy and apoptosis. Lethal autophagy was triggered by RSV higher than 55 μM. The relationship between autophagy and apoptosis depended on the type of autophagy. Specifically, mutual promotion was observed between apoptosis and lethal autophagy. Conversely, cytoprotective autophagy facilitated apoptosis but was unaffected by apoptosis. RSV enhanced NGFR by increasing mRNA expression and prolonging the lifespan of NGFR mRNA and proteins. RSV antagonized the enhanced autophagy and apoptosis caused by NGFR knockdown. As the downstream pathway of NGFR, AMPK-mTOR played a positive role in RSV-induced autophagy and apoptosis. Overall, RSV-induced autophagy and apoptosis in A549 cells are regulated by the NGFR-AMPK-mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 50%

Resveratrol Induces Autophagy and Apoptosis in Non-Small-Cell Lung Cancer Cells by Activating the NGFR-AMPK-mTOR Pathway

Fan

Zhang

et al. 2022

Nutrients

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“…In our study, following HMF treatment, the protein expression levels of p-AMPK, which promotes cell death, and the protein levels of the phosphorylated form of P70S6K and S6 were remarkably inhibited in 5-8F and CNE-2 cells. This observation is consistent with those of previous studies which reported that the AMPK and mTOR pathways might interact in inhibiting the proliferation and inducing the apoptosis of cancer cells, such as colorectal cancer ( Dutta et al, 2022 ), breast cancer ( Li et al, 2021 ), and lung cancer ( Song et al, 2021 ). For instance, the volatile components of frankincense, pine needle, and geranium inhibited the activity, proliferation, migration, and invasion and induced apoptosis of McF-7 human breast cancer cells.…”

Section: Discussionsupporting

confidence: 93%

The molecular mechanism for inhibiting the growth of nasopharyngeal carcinoma cells using polymethoxyflavonoids purified from pericarp of Citrus reticulata ‘Chachi’ via HSCCC

Yang¹,

Liang²,

Liu³

et al. 2023

Front. Pharmacol.

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Polymethoxyflavonoids (PMFs), the main bioactive compounds naturally occurring in the pericarp of Citrus reticulata ‘Chachi’ (CRCP), possess significant antitumor action. However, the action of PMFs in nasopharyngeal carcinoma (NPC) is currently unknown. The present research study was conducted to investigate the inhibitory mechanisms of PMFs from CRCP on NPC growth in vivo and in vitro. In our research, we used high-speed counter-current chromatography (HSCCC) to separate four PMFs (nobiletin (NOB), 3,5,6,7,8,3′,4′-heptamethoxyflavone (HMF), tangeretin (TGN), and 5-hydroxy-6,7,8,3′,4′-pentamethoxyflavone (5-HPMF)) from CRCP. CCK-8 assay was used to preliminarily screen cell viability following exposure to the four PMFs. Colony formation, Hoechst-33258 staining, transwell, and wound scratch assays were performed to assess the anti-proliferation, invasion, migration, and apoptosis-inducing effects of HMF on NPC cells. NPC tumors in xenograft tumor transplantation experiments were also established to explore the effect of HMF (100 and 150 mg/kg/day) on NPC. The histopathological changes in the treated rats were observed by H&E staining and Ki-67 detection by immunohistochemical techniques. The expressions of P70S6K, p-P70S6K, S6, p-S6, COX-2, p53, and p-p53 were measured by Western blot. The four PMFs were obtained with high purity (>95.0%). The results of the preliminary screening by CCK-8 assay suggested that HMF had the strongest inhibitory effect on NPC cell growth. The results of the colony formation, Hoechst-33258 staining, transwell, and wound scratch assays indicated that HMF had significant anti-proliferation, invasion, migration, and apoptosis-inducing ability in NPC cells. Moreover, HMF suppressed NPC tumor growth in xenograft tumor transplantation experiments. Further investigation suggested that HMF regulated NPC cells proliferation, apoptosis, migration, and invasion by activating AMPK-dependent signaling pathways. In conclusion, HMF-induced AMPK activation inhibited NPC cell growth, invasion, and metastatic potency by downregulating the activation of the mTOR signaling pathway and COX-2 protein levels, as well as enhancing the p53 phosphorylation level. Our study provides a crucial experimental basis for the clinical treatment of NPC, as well as the development and utilization of PMFs from CRCP.

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“… [14] Coxsackievirus B3 (CVB3) CVB3 is a potent oncolytic virus for KRAS-mutant lung adenocarcinoma-targeted therapy. [15] microRNA-modified CVB3 (miR-CVB3) miR-CVB3 retains the ability to infect and lyse KRAS-mutant lung adenocarcinoma and TP53/RB1-mutant SCLC cells [16] , [17] EHV-1 Animal virus EHV-1 replicates efficiently in a human adenocarcinoma cell line (A549) [18] Oncopox-trail The TRAIL protein mainly induces apoptosis and inhibits necrosis, and the oncolytic poxviruses carrying the trail gene have better cytotoxicity [19] CF33-GFP Infiltration of tumors by CD8+ T cells [20] Bovine Herpesvirus 1 (BoHV-1) BoHV-1 infection of tumors reduces their protein levels of histone deacetylase (HDAC) by inducing DNA damage [21] Low pathogenic oncolytic influenza virus IAV IAV infection of Raf-BxB mice leads to reversal of immunosuppressed tumor-associated lung macrophage function to an M1-like pro-inflammatory active phenotype [22] Measles virus (MV) vaccine strains MV oncolysis is associated with in vivo activation of caspase-3 [23] Oncolytic myxoma virus (MYXV) Tumor-specific viral replication, induction of tumor necrosis, and growth inhibition-associated cytotoxic immune cell infiltration [24] Oncolytic adenovirus H101 Very potent cytotoxicity, G2/M phase arrest, and cell lysis and inhibition of tumor growth, [25] Recombinant oncolytic adenovirus Ad-apoptin Ad-apoptin targets AMPK and inhibits glycolysis, migration, and invasion of lung cancer cells through the AMPK/mTOR signaling pathway [26] …”

Section: How Does Ov Work In Lung Cancer?mentioning

confidence: 99%

Lung cancer and oncolytic virotherapy——enemy's enemy

Zhang

et al. 2023

Translational Oncology

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Ad-apoptin inhibits glycolysis, migration and invasion in lung cancer cells targeting AMPK/mTOR signaling pathway

Cited by 15 publications

References 29 publications

Resveratrol Induces Autophagy and Apoptosis in Non-Small-Cell Lung Cancer Cells by Activating the NGFR-AMPK-mTOR Pathway

Resveratrol Induces Autophagy and Apoptosis in Non-Small-Cell Lung Cancer Cells by Activating the NGFR-AMPK-mTOR Pathway

The molecular mechanism for inhibiting the growth of nasopharyngeal carcinoma cells using polymethoxyflavonoids purified from pericarp of Citrus reticulata ‘Chachi’ via HSCCC

Lung cancer and oncolytic virotherapy——enemy's enemy

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