PM2.5 exposure-induced autophagy is mediated by lncRNA loc146880 which also promotes the migration and invasion of lung cancer cells

Deng, Xiaobei; Feng, Na; Zheng, Min; Ye, Xiaofei; Lin, Hongyan; Yu, Xiao; Gan, Zhihua; Zheng, Fang; Zhang, Huan; Gao, Ming; Zheng, Zhi; Yu, Herbert; Ding, Wenjun; Qian, Biyun

doi:10.1016/j.bbagen.2016.11.009

Cited by 105 publications

(66 citation statements)

References 52 publications

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“…We previously reported that in lung cancer cells, ROSactivated autophagy promoted EMT, cell migration and invasion, and PM2.5 could increase ROS-activated autophagy. In addition, a lncRNA, LOC146880, was found to play a crucial role in this process [24]. In the current study, by adding CSE and PM2.5 together with si-Atg5, we found that si-Atg5 abolished the effects of CSE and PM2.5 on cell migration, invasion and EMT.…”

Section: Discussionmentioning

confidence: 54%

“…We previously found that lncRNA LOC146880 was up-regulated in lung cancer cells after treatment with PM2.5. LOC146880 knockdown could reverse PM2.5 induced autophagy and malignant behaviors of lung cancer cells [24]. In the previous study, we also found that lncRNA ENST00000439577 located at 1p36.13 was associated with lung cancer survival and ENST00000439577 knockdown in lung cancer cells led to decreased cell proliferation, migration, and invasion (we termed it LCPAT1).…”

Section: Introductionmentioning

confidence: 92%

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LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2

Lin

Zhang

Feng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ecological studies have shown that air pollution and prevalence of cigarette smoking are positively correlated. Evidence also suggests a synergistic effect of cigarette smoking and PM2.5 exposure (Environmental Particulate Matter ≤ 2.5 µm in diameter) on lung cancer risk. We aimed to evaluate the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality and determine its underlying mechanisms in vitro. Methods: “MOVER” method was used to analyze the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality. Cell autophagy and malignant behaviors induced by cigarette smoke extract (CSE) and PM2.5 exposure were examined in vitro. Gene expression was examined by qRT-PCR and western blot. RNA and protein interaction was determined using a RNA binding protein immunoprecipitation assay. Results: An increased risk for lung cancer death (RERI (the relative excess risk) =0.28) was observed with a synergistic interaction between cigarette smoking and PM2.5 pollution. Cell migration, invasion, EMT (epithelial-mesenchymal transition) and autophagy were elevated when lung cancer cells were treated with CSE and PM2.5 in combination. A lncRNA, named lung cancer progression-association transcript 1 (LCPAT1), was up-regulated after the treatment of CSE and PM2.5, and knocking down the lncRNA impaired the effect of CSE and PM2.5 on lung cancer cells. In addition, LCPAT1 was shown to bind to RCC2, and RCC2 mediated the effect of LCPAT1 on cell autophagy, migration, invasion and EMT in lung cancer. Conclusions: Our results suggest that combined exposure to CSE and PM2.5 induces LCPAT1 expression, which up-regulates autophagy, and promotes lung cancer progression via RCC2.

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Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 92%

LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2

Lin

Zhang

Feng

et al. 2018

Cell Physiol Biochem

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“…RNA extraction and analysis were performed as previously described 4,5,22 . The current study was approved by the medical ethical review committees at TMUCIH and Shanghai Jiao Tong University School of Medicine.…”

Section: Methodsmentioning

confidence: 99%

“…The overexpression of the lncRNA BANCR results in an increase in the ratio of LC3II-to-LC3I, which indicates the formation of an autophagosome 21 . Our previous study revealed that the lncRNA LOC146880 participates in PM 2.5 exposure-induced autophagy in lung cancer 4 . The purpose of the current study was to determine the role of LCPAT1 in regulating autophagy in vivo and in vitro .…”

Section: Introductionmentioning

confidence: 97%

Knockdown of long non-coding RNA LCPAT1 inhibits autophagy in lung cancer

Lin

et al. 2018

Cancer Biology & Medicine

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Objective:Long non-coding RNAs (lncRNAs) are involved in numerous biological processes in lung cancer cells. In our previous studies, we identified a lncRNA, ENST00000439577, which is highly expressed in lung carcinomas, and termed it lung cancer progression-associated transcript 1 (LCPAT1). To characterize the role of LCPAT1 in lung cancer, we conducted the current study. Methods:Expression of LCPAT1 and autophagy-associated markers in tumor tissues and lung cancer cell lines was determined by real-time quantitative polymerase chain reaction (qPCR). Hematoxylin and eosin (HE) staining, qPCR, Western blot, and immunohistochemistry were performed to evaluate xenografted tumor tissues. Autophagy induced by rapamycin was detected by Western blot and immunofluorescence in lung cancer cell lines. Results:Expression of LCPAT1 and microtubule-associated protein 1 light chain 3 beta (LC3B) was positively correlated in lung cancer. Knockdown of LCPAT1 inhibited tumor growth and suppressed cell autophagy in vivo. Moreover, LCPAT1 knockdown in lung cancer cell lines resulted in decreased autophagy-associated gene expression and alleviated the cell autophagy induced by rapamycin. Conclusions:We speculate that LCPAT1 plays a crucial role in regulating autophagy in lung cancer.

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“…lncRNA Profiling in Serum A positive correlation between lncRNA loc146880 expression and lc3b levels in tumor tissues and serum of lung cancer patients was reported by Deng and his colleagues [52]. Another scientist Tantai [53] reported that the levels of XIST and HIF1A-AS1 were significantly increased in tumor tissues or serum from NSCLC patients.…”

Section: Whole Blood and Lncrna Profilingmentioning

confidence: 99%

Diagnostic and Prognostic Potential of Circulating Long Non-Coding RNAs in Non Small Cell Lung Cancer

Peng

Wang

Shan

et al. 2018

Cell Physiol Biochem

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Lung cancer is the leading cause of cancer-related mortality worldwide. Approximately 80% of lung cancer cases are non–small cell lung carcinoma (NSCLC). However current diagnostic and therapeutic modalities against NSCLC are ineffective due to incomplete understanding of molecular pathogenesis of NSCLC. Emerging evidence shows that long non-coding RNAs (lncRNAs) can function as biomarkers for diagnosis and prognosis. LncRNAs can control transcription, translation, and protein function via diverse mechanisms although they lack the protein coding potential. LncRNAs have attracted intense investigations on their roles in cancer. Mounting evidence indicates that lncRNAs are promising biomarkers in diagnosis and prognosis for NSCLC, especially their presence in body fluids. Herein we will review recent advances in the research that explores the diagnostic and prognostic potentials of lncRNAs in NSCLC. We will also discuss emerging evidence that suggested lncRNAs as therapeutic targets in NSCLC.

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PM2.5 exposure-induced autophagy is mediated by lncRNA loc146880 which also promotes the migration and invasion of lung cancer cells

Cited by 105 publications

References 52 publications

LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2

LncRNA LCPAT1 Mediates Smoking/ Particulate Matter 2.5-Induced Cell Autophagy and Epithelial-Mesenchymal Transition in Lung Cancer Cells via RCC2

Knockdown of long non-coding RNA LCPAT1 inhibits autophagy in lung cancer

Diagnostic and Prognostic Potential of Circulating Long Non-Coding RNAs in Non Small Cell Lung Cancer

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