Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin β1/ Src signaling in triple negative breast cancer cells

Hamurcu, Zühal; Delibaşı, Nesrin; Geçene, Seda; Şener, Elif Funda; Dönmez-Altuntaş, Hamiyet; Özkul, Yusuf; Canatan, Halit; Özpolat, Bülent

doi:10.1007/s00432-017-2557-5

Cited by 95 publications

(77 citation statements)

References 56 publications

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“…Cell autophagy plays a momentous role in maintaining the stable structure and function of normal glomerular podocytes and proximal renal tubular epithelial cells [10]. Beclin-1 is a homologous gene of yeast autophagy gene Atg6/Vps30, which is one of the essential molecules of the formation of autophagosome [11]. LC3 is involved in the formation of autophagy, has been proved to be one of the common autophagosome marker proteins in mammalian cells [11].…”

Section: Introductionmentioning

confidence: 99%

“…Beclin-1 is a homologous gene of yeast autophagy gene Atg6/Vps30, which is one of the essential molecules of the formation of autophagosome [11]. LC3 is involved in the formation of autophagy, has been proved to be one of the common autophagosome marker proteins in mammalian cells [11]. JNK and mTOR pathways have been testified to join in regulating cell apoptosis and autophagy in diverse diseases and also present the vital roles in the pathophysiology of DN [12,13].…”

Section: Introductionmentioning

confidence: 99%

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Arbutin protects HK-2 cells against high glucose-induced apoptosis and autophagy by up-regulating microRNA-27a

Zhang

Tian³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Arbutin (ARB) has been widely used in skin pigmentation disorders. Nevertheless, the involvements of ARB in diabetic nephropathy (DN) are still unknown. We investigated the functions of ARB in high glucose (HG)-induced cell apoptosis and autophagy in HK-2 cells. Cell viability was examined through CCK-8 in HK-2 cells after disposal with 45 mM glucose and ARB (10-50 lM). Flow cytometry and western blot tested cell apoptosis and the related protein levels in HK-2 cells after 45 mM glucose and 50 lM ARB administration. RT-qPCR delved microRNA (miR)-27a expression in HG and ARB co-treated HK-2 cells. Effect of miR-27a on ARB affected cell apoptosis and autophagy was investigated after miR-27a inhibitor transfection. JNK and mTOR pathways were finally assessed by western blot. ARB alleviated HG-induced cell apoptosis, autophagy and regulated the related protein levels in HK-2 cells. MiR-27a expression was reduced in HG-treated cells, but was accelerated in HG and ARB co-treated HK-2 cells with the increased concentration. Inhibition of miR-27a apparently abolished the outcomes of ARB in HG-induced HK-2 cells apoptosis and autophagy. Besides, ARB blocked JNK and mTOR pathways by regulating miR-27a. The findings demonstrated that ARB alleviated apoptosis and autophagy in HGtreated HK-2 cells by regulating miR-27a/JNK/mTOR axis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Arbutin protects HK-2 cells against high glucose-induced apoptosis and autophagy by up-regulating microRNA-27a

Zhang

Tian³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…2 Beijing National Biochip Research Center Sub-Center in Ningxia, The General Hospital of Ningxia Medical University, Yinchuan 750004, China. 3 Medical Animal Lab, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.…”

Section: Author Detailsmentioning

confidence: 99%

“…And the incidence and mortality of breast cancer have increased by nearly 18% since 2008 [2]. Breast cancer is a diverse hormone-dependent carcinoma, with both genetic and epigenetic changes leading to initiation, progression and metastasis [3]. Despite significant advances have been made in the biological development of breast cancer, the occurrence of metastasis still leads to poor prognosis and low survival.…”

Section: Introductionmentioning

confidence: 99%

PGC-1β cooperating with FOXA2 inhibits proliferation and migration of breast cancer cells

Cao¹,

Wang²,

Wang³

et al. 2019

Cancer Cell Int

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Background: Breast cancer is one of the most common malignancy among females from the worldwide cancer incidence statistics. Peroxisome gamma coactivator-1β (PGC-1β) has long been identified to be involved in this type of tumorigenesis. However, the mechanisms of PGC-1β in human breast cancer have not been fully understood and the function requires to be further elucidated. Methods: mRNA and protein expression of PGC-1β and FOXA2 in breast cancer tissues and cell lines were determined by qRT-PCR and Western Blotting, respectively. To further visualize the expression and localization of PGC-1β and FOXA2, immunochemistry and immunofluorescence staining methods were employed. The effect of PGC-1β and FOXA2 on cell proliferation and migration were evaluated by CCK8, clone formation, transwell and wound-healing assays, which has been done either with stable PGC-1β knockdown or FOXA2 overexpression in vitro. Xenografts model of nude mice were used to evaluate tumor growth in vivo. In addition, proteins expression of the PI3K-AKT-mTOR signaling pathway involved in the regulation of breast cancer were detected by Western Blotting. Results: Our results showed that PGC-1β was upregulated and FOXA2 was downregulated in breast cancer tissues and cell lines. These two proteins can be interacted with each other to form the complex. Also, we found the combination of PGC-1β interference with FOXA2 overexpression significantly inhibited cell proliferation and migration in vitro as well as tumor growth in vivo. We further identified that PGC-1β and FOXA2 strongly correlated with the PI3K-AKT-mTOR signaling pathway, and they exerted their biological functions by activating this pathway. Conclusions: We demonstrated that downregulation of PGC-1β combined with overexpression of FOXA2 obviously inhibited the function of breast cancer cells through regulating the PI3K-AKT-mTOR pathway.

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“…Additionally, in disease conditions of myocardial ischemia-reperfusion and neuronal ischemic anoxia, autophagy enhancement serves a role as a protective mechanism (37). Recent studies (38,39) have shown that drug-induced autophagy is characterized by the altered expression of autophagy-associated proteins LC3 and beclin1. LC3 and beclin1 are two pacemakers in the autophagic cascade.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of extracellular polymeric substances from Aphanizomenon�flos‑aquae on neurotoxicity induced by local anesthetics

Xue

Leng

et al. 2018

Exp Ther Med

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The neurotoxicity of local anesthetics has received an increasing amount of attention and more effective therapeutic agents are required. Extracellular polymeric substances from Aphanizomenon flos-aquae (EPS-A) are high molecular weight polysaccharides. The present study aimed to elucidate the protective effects of EPS-A on neurotoxicity induced by local anesthetics in an intraperitoneal injection bupivacaine rat model. The results of immunohistochemical staining inicated that following intraperitoneal injection of EPS-A the levels of apoptosis and caspase-3 decreased, and the expression levels of microtubule-associated protein 1A light chain 3 (LC3) and beclin1 increased. In order to further clarify the mechanism of the EPS-A-mediated protection, the expression of key proteins associated with autophagy was investigated by western blotting. The results suggested that the ratio of LC3-II/LC3-I and the expression level of beclin1 increased. Taken together, the results indicated that EPS-A induced neuroprotective effects on bupivacaine-induced neurotoxicity. The underlying mechanism may be associated with the inhibition of apoptosis, upregulation of autophagy and improvement of cell survival. The results suggested that EPS-A may be a candidate neuroprotective agent against neurotoxicity caused by local anesthetics.

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Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin β1/ Src signaling in triple negative breast cancer cells

Cited by 95 publications

References 56 publications

Arbutin protects HK-2 cells against high glucose-induced apoptosis and autophagy by up-regulating microRNA-27a

Arbutin protects HK-2 cells against high glucose-induced apoptosis and autophagy by up-regulating microRNA-27a

PGC-1β cooperating with FOXA2 inhibits proliferation and migration of breast cancer cells

Protective effects of extracellular polymeric substances from Aphanizomenon�flos‑aquae on neurotoxicity induced by local anesthetics

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