Linna Tan
Central South University
5 Papers
4 Citations
Linna Tan is an academic researcher from Central South University. The author has contributed to research in topics: Cancer & Chemistry. The author has an hindex of 2, co-authored 5 publications.
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Papers
Endoscopic resection of gastric gastrointestinal stromal tumors.
TL;DR: This review summarizes the recent advances on endoscopic resection of gastric GISTs, aiming to provide a rational management strategy for gastrointestinal stromal tumors.
•Journal Article
SET7 interacts with HDAC6 and suppresses the development of colon cancer through inactivation of HDAC6.
Shi-Lan Zhang,Xiao Du,Linna Tan,Feihong Deng,Bing-Yi Zhou,Hejun Zhou,Hongyi Zhu,Yi Chu,Deliang Liu,Yuyong Tan +9 more
TL;DR: SET7 is a promising therapeutic target for preventing metastasis and improving prognosis in colon cancer, and its interaction effect significantly decreased the ratios of p-ERK/ERK, which indicated that it may partly suppress ERK signaling pathway.
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Factors that predict the technical difficulty during endoscopic full-thickness resection of a gastric submucosal tumor
Gong Jian,Linna Tan,Hanyu Wang,Liang Lv,Xuehong Wang,Xiaoyun Qi,Meixian Le,Yuyong Tan,Deliang Liu +8 more
TL;DR: EFTR is safe and effective for the treatment of gastric SMTs and risk factors for technical difficulty, such as gender, age, tumor location, size, symptomatic, regular, outgrowth, operator experience and pathology were analyzed.
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Single tunnel-assisted endoscopic submucosal dissection for a 13-cm giant colorectal laterally spreading tumor.
TL;DR: An en bloc resection of a 60-year-old male with a giant colorectal laterally spreading tumor at the recto-sigmoid junction was achieved with no perforation or post-operative bleeding and a comparatively low procedure time.
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Functions of ULK1 in autophagy and non-autophagy pathways and its implications in human physiology and disease
Linna Tan,Yuyong Tan,Deliang Liu +2 more
Abstract: ULK1 (unc-51 like autophagy activating kinase 1), a mammalian serine/threonine kinase, is a key component of autophagy initiation complex and helps to induce all types of autophagy. Canonical autophagy is a process in which, through the interactions of a series of autophagy-related proteins, damaged organelles or misfolded proteins are engulfed by autophagosomes and then merged with lysosomes to be degraded. Thus, canonical autophagy is an important constituent part of the cellular “quality control.” Besides, accumulating evidence indicates that ULK1 exerts autophagy-independent effects in a cell-specific manner. For example, ULK1 facilitates neurite elongation through the regulation of endoplasmic reticulum (ER)–Golgi trafficking in neurons, stimulates phosphopentose pathway to help NADPH (nicotinamide adenine dinucleotide phosphate hydrogen) production, and acts as a duplex regulator in type I IFN (type I interferon) induced innate immune response. Considering the importance and diversity of ULK1 in various biological processes, this review aims to present a comprehensive overview of autophagy and non-autophagy related functions of ULK1 in a variety of human physiological, pathological, and disease processes.
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