Correction

Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p (vol 16, pg 118, 2017)

MOLECULAR CANCER (2017)

Get Full Text
Add to Collection

Journal

MOLECULAR CANCER
Volume 16, Issue -, Pages -

Publisher

BIOMED CENTRAL LTD
DOI: 10.1186/s12943-017-0716-6

Keywords

-

Categories

Biochemistry & Molecular Biology Oncology

Ask authors/readers for more resources

Protocol

Community support

Reagent

Community support

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Recommended

Article Biochemistry & Molecular Biology

ANKRD13a controls early cell-death checkpoint by interacting with RIP1 independent of NF-κB

Minho Won, Kyeong Ah Park, Sup Kim, Eunjin Ju, Youngbok Ko, Heonjong Yoo, Hyunju Ro, Jaeseob Lee, Junseo Oh, Eun Gyo Lee, Sang Yean Kim, Suk Woo Nam, Han-Ming Shen, Min-Kyung Yeo, Jin Man Kim, Gang Min Hur

Summary: The study shows that ANKRD13a is a novel component in TNF signaling, influencing the threshold of cell death signals and reducing the risk of cell death. Lack of ANKRD13a promotes the formation of complex-II, shifting cell response from survival to death without affecting NF-κB activation.

CELL DEATH AND DIFFERENTIATION (2022)

Add to Collection
Article Biochemical Research Methods

O-GlcNAcylation promotes fatty acid synthase activity under nutritional stress as a pro-survival mechanism in cancer cells

Yin-Kwan Wong, Jigang Wang, Teck Kwang Lim, Qingsong Lin, Celestial T. Yap, Han-Ming Shen

Summary: This study provides new insights into the role of O-GlcNAcylation in the stress response, specifically in the context of cellular starvation. It highlights the protective effects of O-GlcNAcylation under starvation conditions and suggests the potential of combining inhibition of O-GlcNAcylation and fatty acid synthase (FASN) in cancer therapy, as dual inhibition showed a synergistic effect in inducing cancer cell death.

PROTEOMICS (2022)

Add to Collection
Article Pharmacology & Pharmacy

Celastrol induces ferroptosis in activated HSCs to ameliorate hepatic fibrosis via targeting peroxiredoxins and HO-1

Piao Luo, Dandan Liu, Qian Zhang, Fan Yang, Yin-Kwan Wong, Fei Xia, Junzhe Zhang, Jiayun Chen, Ya Tian, Chuanbin Yang, Lingyun Dai, Han-Ming Shen, Jigang Wang

Summary: Celastrol exerts anti-fibrotic effects by inducing ferroptosis and promoting the production of ROS. It directly binds to PRDXs and HO-1, inhibiting their antioxidant activities and increasing ROS levels, thereby inducing ferroptosis.

ACTA PHARMACEUTICA SINICA B (2022)

Add to Collection
Review Pharmacology & Pharmacy

Impairment of the autophagy-lysosomal pathway in Alzheimer's diseases: Pathogenic mechanisms and therapeutic potential

Wei Zhang, Chengchao Xu, Jichao Sun, Han-Ming Shen, Jigang Wang, Chuanbin Yang

Summary: Alzheimer's disease is a common neurodegenerative disorder characterized by memory loss and cognitive dysfunction. Impaired autophagy-lysosomal pathway is linked to AD pathogenesis, and enhancing autophagy to remove protein aggregates is proposed as a promising therapeutic strategy.

ACTA PHARMACEUTICA SINICA B (2022)

Add to Collection
Article Engineering, Biomedical

Amelioration of Alzheimer's disease pathology by mitophagy inducers identified via machine learning and a cross-species workflow

Chenglong Xie, Xu-Xu Zhuang, Zhangming Niu, Ruixue Ai, Sofie Lautrup, Shuangjia Zheng, Yinghui Jiang, Ruiyu Han, Tanima Sen Gupta, Shuqin Cao, Maria Jose Lagartos-Donate, Cui-Zan Cai, Li-Ming Xie, Domenica Caponio, Wen-Wen Wang, Tomas Schmauck-Medina, Jianying Zhang, He-ling Wang, Guofeng Lou, Xianglu Xiao, Wenhua Zheng, Konstantinos Palikaras, Guang Yang, Kim A. Caldwell, Guy A. Caldwell, Han-Ming Shen, Hilde Nilsen, Jia-Hong Lu, Evandro F. Fang

Summary: This study utilized machine learning and a cross-species approach to identify and validate two potent mitophagy inducers. These compounds improved neuronal survival and functionality, abrogated pathology in AD models, and enhanced memory.

NATURE BIOMEDICAL ENGINEERING (2022)

Add to Collection
Article Cell Biology

WIPI2 positively regulates mitophagy by promoting mitochondrial recruitment of VCP

Guang Lu, Hayden Weng Siong Tan, Tomas Schmauck-Medina, Liming Wang, Jiaqing Chen, Yik-Lam Cho, Kelie Chen, Jing-Zi Zhang, Weifeng He, Yihua Wu, Dajing Xia, Jing Zhou, Evandro F. Fang, Lei Fang, Wei Liu, Han-Ming Shen

Summary: This study reveals the crucial role of WIPI2 in mitochondrial recruitment of VCP to promote outer mitochondrial membrane protein degradation and eventual mitophagy. WIPI2 is recruited to damaged mitochondria upon mitophagy induction and its loss impairs mitophagy induced by mitochondrial damaging agents. WIPI2 binds to and promotes the transportation of AAA-ATPase VCP/p97 to damaged mitochondria, and its depletion blunts the recruitment of VCP to damaged mitochondria, leading to reduction in degradation of outer mitochondrial membrane proteins and mitophagy. Furthermore, WIPI2 is implicated in cell fate decision as cells deficient in WIPI2 are largely resistant to cell death induced by mitochondrial damage.

AUTOPHAGY (2022)

Add to Collection
Article Biochemistry & Molecular Biology

NAMPT mitigates colitis severity by supporting redox-sensitive activation of phagocytosis in inflammatory macrophages

A-Yeon Lee, Sung-Min Hwang, Yu-Jin Ha, Moo-Jin Kim, Seongki Min, Won Hwang, Gyesoon Yoon, Hee-Hoon Kim, Won-Il Jeong, Han-Ming Shen, Sin-Hyeog Im, Dakeun Lee, You-Sun Kim, Sun Mi Hong, So Mee Kwon, Hyun Goo Woo

Summary: This study investigates the role of Nicotinamide phosphoribosyltransferase (NAMPT) in inflammatory macrophages, particularly in the context of inflammatory bowel disease (IBD). The findings suggest that insufficient NAD(+) levels due to NAMPT deficiency in macrophages lead to reduced phagocytic activity and prolonged chronic colitis. Nicotinamide mononucleotide (NMN) treatment can rescue NADPH levels and effectively suppress the severity of DSS-induced colitis.

REDOX BIOLOGY (2022)

Add to Collection
Article Cell Biology

PFKP alleviates glucose starvation-induced metabolic stress in lung cancer cells via AMPK-ACC2 dependent fatty acid oxidation

Jiaqing Chen, Li Zou, Guang Lu, Oleg Grinchuk, Lei Fang, Derrick Sek Tong Ong, Reshma Taneja, Choon-Nam Ong, Han-Ming Shen

Summary: This study reveals the important role of PFKP in non-small-cell lung cancer (NSCLC), showing that PFKP interacts with AMPK to promote mitochondrial recruitment of AMPK and enhance phosphorylation of ACC2, ultimately promoting long-chain fatty acid oxidation and cancer cell survival under glucose starvation.

CELL DISCOVERY (2022)

Add to Collection
Editorial Material Cell Biology

Targeting mitophagy to promote apoptosis is a potential therapeutic strategy for cancer

Yancheng Tang, Liming Wang, Jiangjiang Qin, Yingying Lu, Han-Ming Shen, Hu-Biao Chen

Summary: Inhibition of PINK1-PRKN-mediated mitophagy enhances the anticancer efficacy of magnolol and could be a promising therapeutic strategy for overcoming cancer drug resistance and improving the therapeutic efficacy of anticancer agents.

AUTOPHAGY (2023)

Add to Collection
Article Cell Biology

Modulation of Atg genes expression in aged rat liver, brain, and kidney by caloric restriction analyzed via single-nucleus/cell RNA sequencing

Chuanbin Yang, Siyu Xia, Wei Zhang, Han-Ming Shen, Jigang Wang

Summary: Using single-cell RNA sequencing, this study found that the transcription patterns of Atg genes in different cell types of rat liver, brain, and kidney are highly heterogeneous. Caloric restriction can reverse the changes of these genes during aging.

AUTOPHAGY (2023)

Add to Collection
Editorial Material Cell Biology

Autophagic secretion of mitochondria (ASM): an alternative way for getting rid of damaged mitochondria

Hayden Weng Siong Tan, Guang Lu, Han-Ming Shen

Summary: PINK1-PRKN-mediated mitophagy is an important pathway for mitochondrial quality control. Our study reveals that the mATG8 conjugation system is not necessary for PINK1-PRKN-mediated mitochondria clearance, and instead, clearance is achieved through secretory autophagy.

AUTOPHAGY (2023)

Add to Collection
Review Cell Biology

The emerging mechanisms and functions of microautophagy

Liming Wang, Daniel J. Klionsky, Han-Ming Shen

Summary: Microautophagy is a type of autophagy that involves the direct engulfment of cytoplasmic components by lysosomes and late endosomes. Although it has only recently emerged as an important cellular process, microautophagy plays a critical role in diseases and provides potential targets for intervention strategies.

NATURE REVIEWS MOLECULAR CELL BIOLOGY (2023)

Add to Collection
Editorial Material Cell Biology

Targeting mitophagy as a novel therapeutic approach in liver cancer

Ji Feng, Jing Zhou, Yong Wu, Han-Ming Shen, Tao Peng, Guo-Dong Lu

Summary: Ischemia is a common pathological process that restricts nutrient availability and induces autophagy. Although autophagy helps sustain nutrient/energy and restrict damages in short-term scenarios, it leads to cell death in long-term scenarios. Ischemia has been used as a clinical application for cancer treatment, but its efficacy is limited. Our recent research shows that combining sorafenib with glucose starvation can enhance cell death in hepatocellular carcinoma (HCC) by impairing mitophagy. We also identified SIAH1 as an important E3 ubiquitin ligase for mitophagic induction in HCC cells.

AUTOPHAGY (2023)

Add to Collection
Article Geriatrics & Gerontology

Morusin and mulberrin extend the lifespans of yeast and C. elegans via suppressing nutrient-sensing pathways

Pingkang Xu, Qimin Chen, Xiaoman Chen, Hao Qi, Yuyan Yang, Weiqi Li, Xin Yang, Amelia Gunawan, Shuoyu Chen, Huimin Zhang, Han-Ming Shen, Dejian Huang, Brian Kennedy, Li Xu, Ziyun Wu

Summary: This study demonstrates that morusin and mulberrin can extend the lifespan of yeast and C. elegans by targeting SCH9 and akt-1 or akt-2 genes, respectively. Additionally, they exhibit other benefits in worms and slow cell senescence in HeLa cells.

GEROSCIENCE (2023)

Add to Collection
Article Biochemistry & Molecular Biology

STING directly recruits WIPI2 for autophagosome formation during STING-induced autophagy

Wei Wan, Chuying Qian, Qian Wang, Jin Li, Hongtao Zhang, Lei Wang, Maomao Pu, Yewei Huang, Zhengfu He, Tianhua Zhou, Han-Ming Shen, Wei Liu

Summary: The cGAS-STING pathway plays a crucial role in host defense by sensing pathogen DNA and inducing immune responses. In this study, it was discovered that STING directly interacts with WIPI2, a key protein involved in autophagy. This interaction is necessary for the formation of autophagosomes induced by STING, but does not affect the activation and trafficking of STING. Furthermore, the specific interaction between STING and WIPI2 leads to competition with PI3P binding, resulting in mutual inhibition between STING-induced autophagy and canonical PI3P-dependent autophagy.

EMBO JOURNAL (2023)

Add to Collection
No Data Available
Webinars Posters Questions Hubs Funding Journals Papers Connect Collections Reviewers About Us FAQs Mobile App Privacy Policy Terms of Use
© Peeref 2019-2024. All rights reserved.