Autophagy facilitates TLR4- and TLR3-triggered migration and invasion of lung cancer cells through the promotion of TRAF6 ubiquitination

Zhan, Zhenlin; Xie, Xuefeng; Cao, Hao; Zhou, Xiaohui; Zhang, Xu Dong; Fan, Huimin; Liu, Zhongmin

doi:10.4161/auto.27162

Cited by 175 publications

(204 citation statements)

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“…Knockdown of ATG7 strongly enhanced the apoptosis induced by various anticancer agents including tyrosine kinase inhibitors [18][19][20]. Recent studies showed that autophagy may promote carcinoma cell invasion and correlate with poor prognosis in cholangiocarcinoma [21,22]. In this study, we found that blockage of autophagy by downregulation of ATG7 or MARCH7 expression led to the inhibition of TGF-β induced cellular migration and invasion.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 53%

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

Zhang

Mei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ubiquitin E3 ligase MARCH7 plays an important role in T cell proliferation and neuronal development. But its role in ovarian cancer remains unclear. This study aimed to investigate the role of Ubiquitin E3 ligase MARCH7 in ovarian cancer. Methods: Real-time PCR, immunohistochemistry and western blotting analysis were performed to determine the expression of MARCH7, MALAT1 and ATG7 in ovarian cancer cell lines and clinical specimens. The role of MARCH7 in maintaining ovarian cancer malignant phenotype was examined by Wound healing assay, Matrigel invasion assays and Mouse orthotopic xenograft model. Luciferase reporter assay, western blot analysis and ChIP assay were used to determine whether MARCH7 activates TGF-β-smad2/3 pathway by interacting with TGFβR2. Results: MARCH7 interacted with MALAT1 by miR-200a (microRNA-200a). MARCH7 may function as a competing endogenous RNA (ceRNA) to regulate the expression of ATG7 by competing with miR-200a. MARCH7 regulated TGF-β-smad2/3 pathway by interacting with TGFβR2. Inhibition of TGF-β-smad2/3 pathway downregulated MARCH7, MALAT1 and ATG7. MiR-200a regulated TGF-β induced autophagy, invasion and metastasis of SKOV3 cells by targeting MARCH7. MARCH7 silencing inhibited autophagy invasion and metastasis of SKOV3 cells both in vitro and in vivo. In contrast, MARCH7 overexpression promoted TGF-β induced autophagy, invasion and metastasis of A2780 cells in vitro by depending on MALAT1 and ATG7. We also found that TGF-β-smad2/3 pathway regulated MARCH7 and ATG7 through MALAT1. Conclusions: These findings suggested that TGFβR2-Smad2/3-MALAT1/MARCH7/ATG7 feedback loop mediated autophagy, migration and invasion in ovarian cancer.

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Section: Cellular Physiology and Biochemistrysupporting

confidence: 53%

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

Zhang

Mei

et al. 2018

Cell Physiol Biochem

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“…Regarding ovarian tumors, it has been suggested that TLR2, TLR3, TLR4 and TLR5 have high levels of expression in normal ovarian epithelium and epithelial ovarian neoplasms (7). It was also revealed that TLR4 has a high expression level in ovarian granular cells (8).…”

Section: Introductionmentioning

confidence: 99%

Effect of TLR4 on the growth of SiHa human cervical cancer cells via the MyD88‑TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways

Ding

et al. 2018

Oncol Lett

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Abstract. The present study aimed to investigate the effect of Toll-like receptor 4 (TLR4) on SiHa human cervical cancer cells and its potential molecular biological mechanisms. The expression of TLR4 following treatment with lipopolysaccharide (LPS) in in SiHa cervical cancer cells was detected by quantitative polymerase chain reaction (qPCR). LPS-induced cell proliferation and apoptosis were detected by MTT assay as well as staining with propidium iodide (PI) and Annexin V/PI double staining. qPCR was performed to analyze the expression levels of tumor necrosis factor receptor-associated factor 6 (TRAF6) and transforming growth factor-activated kinase 1 (TAK1) genes. Western blot analysis was performed to analyze the expression of myeloid differentiation 88 (MyD88), nuclear factor-κB (NF-κB), cyclin D1 and signal transducer and activator of transcription 3 (STAT3) proteins. In the present study, it was revealed that TLR4 expression in SiHa cervical cancer cells may be upregulated by LPS. Additionally, LPS was able to increase the proliferation of SiHa cells. However, LPS treatment did not have an effect on apoptosis of the cells. In addition, the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways were induced in SiHa cells by LPS. These results suggested the effect of LPS and TLR4 on proliferation of SiHa human cervical cancer cells via the MyD88-TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways.

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“…TLRs are usually expressed in cancer cells and are responsible for the regulation of autophagy as well as several immune responses [11]. Autophagy triggered by TLR3 and TLR4 was shown to contribute to the progression of lung cancer [12]. However, several studies have suggested that TLR activation enhances the survival, proliferation, and metastasis of cancer cells [12,16,17,18,19].…”

Section: Autophagy As An Innate Immune Response Against Cancermentioning

confidence: 99%

“…However, several studies have suggested that TLR activation enhances the survival, proliferation, and metastasis of cancer cells [12,16,17,18,19]. Furthermore, TLRs trigger the release of proinflammatory cytokines, chemokines, and immunosuppressive factors, leading to immune evasion and enhanced cancer cell resistance [12,19].…”

Section: Autophagy As An Innate Immune Response Against Cancermentioning

confidence: 99%

“…TLRs induce inflammatory cytokine production by activating the NF-kB and MAPK pathways, mainly through myeloid differentiation primary response 88 (MYD88)-dependent pathways, either alone or in collaboration with TICAM1 (toll-like receptor adaptor molecule 1) -dependent pathways [12,14,15]. TLRs are usually expressed in cancer cells and are responsible for the regulation of autophagy as well as several immune responses [11].…”

Section: Autophagy As An Innate Immune Response Against Cancermentioning

confidence: 99%

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Molecular interactions of autophagy with the immune system and cancer

Hong¹,

Jin²,

Hong³

et al. 2017

Preprint

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Autophagy is a highly conserved catabolic mechanism that mediates the degradation of damaged cellular components by inducing their fusion with lysosomes. This process provides cells with an alternative source of energy for the synthesis of new proteins and the maintenance of metabolic homeostasis in stressful environments. Numerous studies have demonstrated beneficial roles for the induction as well as the suppression of autophagy in cancer cells. Autophagy may induce either survival or death depending on the cell/tissue type. Radiation therapy is widely used therapeutic option to treat cancer, and it induces autophagy in human cancer cell line. Also, melatonin seems to affect cancer cell death via regulation of programmed cell death. In this review, we summarize the current understanding of autophagy and its regulation in cancer.

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Autophagy facilitates TLR4- and TLR3-triggered migration and invasion of lung cancer cells through the promotion of TRAF6 ubiquitination

Abstract: (2014) Autophagy facilitates TLR4-and TLR3-triggered migration and invasion of lung cancer cells through the promotion of TRAF6 ubiquitination, Autophagy, 10:2, 257-268,

Cited by 175 publications

References 50 publications

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

Effect of TLR4 on the growth of SiHa human cervical cancer cells via the MyD88‑TRAF6-TAK1 and NF-κB-cyclin D1-STAT3 signaling pathways

Molecular interactions of autophagy with the immune system and cancer

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