RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

Shu, Chih‐Wen; Chang, Hong‐Tai; Wu, Chieh‐Shan; Chen, Chien‐Hsun; Wu, Sam; Chang, Hong-Po; Kuo, Soong-Yu; Fu, Earl; Liu, Pei‐Feng; Hsieh, Yao-Dung

doi:10.1371/journal.pone.0160586

Cited by 14 publications

(9 citation statements)

References 46 publications

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“…The ONE-Glo® Luminescent Cell Viability Assay kit (Promega Corporation, Madison, WI, USA) and a Fluoroskan Ascent FL reader (Thermo Fisher Scientific, Waltham, USA) were used for measuring and quantifying the luminescence of the luciferase-based reporter, respectively. CMV constitutive luciferase expression (pGL4.50) was used to normalize luminescent signals 50 .…”

Section: Methodsmentioning

confidence: 99%

HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma

Kang

Shu

Chao

et al. 2019

Sci Rep

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Buccal mucosa squamous cell carcinoma (BMSCC) is one of major subsites of oral cancer and is associated with a high rate of metastasis and poor prognosis. Heat shock proteins (HSPs) act as potential prognostic biomarkers in many cancer types. However, the role of HSPD1 in oral cancer, especially in BMSCC, is still unknown. Through data analysis with The Cancer Genome Atlas (TCGA), we found the association of HSPD1 gene expression with tumorigenesis and poor prognosis in oral cancer patients. Our cohort study showed that higher HSPD1 protein level was associated with tumorigenesis and poor prognosis in BMSCC patients with lymph node invasion, suggesting that HSPD1 may be involved in tumor metastasis. Moreover, knockdown of HSPD1 induced E-cadherin expression and decreased the migration and invasion of BMSCC cells. In contrast, ectopic expression of HSPD1 diminished E-cadherin expression and promoted the migration/invasion of BMSCC cells. Further, HSPD1 regulated RelA activation to repress E-cadherin expression, enhancing the migration and invasion of BMSCC cells. Furthermore, HSPD1 protein level was inversely correlated with E-cadherin protein level in tumor tissues and co-expression of high HSPD1/low E-cadherin showed a significant association with poor prognosis in BMSCC patients. Taken together, HSPD1 might repress E-cadherin expression and promote metastatic characters of BMSCC cells for poor prognosis of BMSCC patients.

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Section: Methodsmentioning

confidence: 99%

HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma

Kang

Shu

Chao

et al. 2019

Sci Rep

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“…A549 cells were treated with or without 20 µM chloroquine for 1 h prior to β-sitosterol treatment and BAMBI transfection. The recovered cell lysates were used to detect the accumulation of LC3 II, autophagic flux were detected by immunoblotting according to a previous study (20), briefly, cells were rinsed with PBS and lysed with an lysis buffer. The proteins were then separated by SDS-PAGE and transferred onto nitrocellulose membranes.…”

Section: Methodsmentioning

confidence: 99%

BAMBI overexpression together with β-sitosterol ameliorates NSCLC via inhibiting autophagy and inactivating TGF-β/Smad2/3 pathway

Wang

et al. 2017

Oncology Reports

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Abstract. Non-small cell lung cancer (NSCLC) has the highest mortality rate among all solid tumors with a poor prognosis. The BMP and activin receptor membrane bound inhibitor (BAMBI) has been identified as a hallmark of NSCLC and β-sitosterol possesses antitumor potentiality. This study explores the effect of BAMBI overexpression and β-sitosterol in the context of NSCLC. The results revealed that the transfection of pcDNA-BAMBI and β-sitosterol treatment significantly reduced the levels of autophagy markers light chain 3 (LC3) II and Beclin 1, whereas the levels of LC3 I and p62 were promoted. The reduced punctate accumulations of GFP-LC3 were detected in pcDNA-BAMBI and β-sitosterol groups, especially in pcDNA-BAMBI + β-sitosterol group. BAMBI overexpression and β-sitosterol induced G0/G1 cell cycle arrest and inhibted cell proliferation in A549 cells. In addition, the levels of transforming growth factor-β (TGF-β)/p-Smad2/3/c-Myc pathway proteins were decreased. The TGF-β overexpression further confirmed that BAMBI overexpression and β-sitosterol treatment suppre ssed autohagy and viability of A549 cells was through TGF-β/Smad2/3/c-Myc pathway. Finally, the tumor growth was suppressed in NSCLC xenografts, and the inhibitory effect was stronger under treatment of pcDNA-BAMBI together with β-sitosterol. These results indicate that BAMBI overexpression and β-sitosterol may serve as novel targets for the treatment of NSCLC. IntroductionLung cancer is the leading cause of deaths with the most rapidly increasing incidence worldwide. Non-small cell lung cancer (NSCLC) has the highest mortality rate among all solid tumors with a poor prognosis (1). More than half of lung carcinomas are detected in a progressed or already metastasized state with a 5-year survival, for lacking of characteristic early symptoms (2). The general therapy treating the majority of patients is chemotherapy, which often induces resistance (3). It is necessary to develop novel therapeutic approaches to better understand the lung cancer progression.Autophagy is a fundamental cellular homeostatic process that cells use to degrade and recycle cellular proteins (4). This process can be induced in response to either intracellular or extracellular factors, such as hypoxia, low cellular energy state and organelle damage (5). The microtubule-associated protein 1 light chain 3 (LC3), functions as a structural component in the formation of autophagosomes. The conversion of the cytosolic form of LC3 (LC3 I) to lipidated form (LC3 II) indicates autophagosome formation (6). Beclin 1, is required for the initiation and in the process of autophagosome formation (7). p62 acts as a receptor or adaptor for autophagic degradation of ubiquitinated proteins, the upregulation of p62 is commonly detected in human tumors and contributes dire ctly to tumorigenesis (8). Thus, LC3, Beclin 1 and p62 were considered as autophagy markers in many studies (9,10).Transforming growth factor-β (TGF-β) has a crucial role in homeostasis, fibrosis angiogenesis, carcinogenesis and d...

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“…Oxidative stress can also stimulate PI3KC3 complex assembly. In cancer cells, mitochondrial ROS produced after low-power laser irradiation have been shown to upregulate BECN1 expression via the rise of p65/RELA transcriptional activity [63] (Figure 3). Furthermore, it has been described that the inhibition of the mitochondrial electron transport chain—with the consequent generation of ROS—promotes the translocation of high mobility group box 1 (HMGB1) protein from the nucleus to the cytosol, where it disrupts the inhibitory interaction of Bcl-2 with BECN1 [64] (Figure 3).…”

Section: Regulation Of Autophagy By Mitochondrial Oxidative Stressmentioning

confidence: 99%

Recent Insights into the Mitochondrial Role in Autophagy and Its Regulation by Oxidative Stress

Roca-Agujetas

Dios

Lestón

et al. 2019

Oxidative Medicine and Cellular Longevity

115

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Autophagy is a self-digestive process that degrades intracellular components, including damaged organelles, to maintain energy homeostasis and to cope with cellular stress. Autophagy plays a key role during development and adult tissue homeostasis, and growing evidence indicates that this catalytic process also has a direct role in modulating aging. Although autophagy is essentially protective, depending on the cellular context and stimuli, autophagy outcome can lead to either abnormal cell growth or cell death. The autophagic process requires a tight regulation, with cellular events following distinct stages and governed by a wide molecular machinery. Reactive oxygen species (ROS) have been involved in autophagy regulation through multiple signaling pathways, and mitochondria, the main source of endogenous ROS, have emerged as essential signal transducers that mediate autophagy. In the present review, we aim to summarize the regulatory function of mitochondria in the autophagic process, particularly regarding the mitochondrial role as the coordination node in the autophagy signaling pathway, involving mitochondrial oxidative stress, and their participation as membrane donors in the initial steps of autophagosome assembly.

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RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

Cited by 14 publications

References 46 publications

HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma

HSPD1 repressed E-cadherin expression to promote cell invasion and migration for poor prognosis in oral squamous cell carcinoma

BAMBI overexpression together with β-sitosterol ameliorates NSCLC via inhibiting autophagy and inactivating TGF-β/Smad2/3 pathway

Recent Insights into the Mitochondrial Role in Autophagy and Its Regulation by Oxidative Stress

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