<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen KD</submitter><funding>Chang Gung Memorial Hospital</funding><pagination>163-168</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6138774</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(3)</volume><pubmed_abstract>The physiological role of autophagy in the catabolic process of the body involves protein synthesis and degradation in homeostasis under normal and stressed conditions. In hepatocellular carcinoma (HCC), the role of tumor microenvironment (TME) has been concerned as the main issue in fighting against this deadly malignancy. During the last decade, the crosstalk between tumor cells and their TME in HCC extensively accumulated. However, a deeper knowledge for the actual function of autophagy in this interconnection which involved in supporting tumor development, progression and chemoresistance in HCC is needed but still largely unknown. Recent studies have shown that coagulants tissue factor (TF) and factor VII (FVII) has a pathological role in promoting tumor growth by activating protease-a</pubmed_abstract><journal>Biomedical journal</journal><pubmed_title>Tumor microenvironment mediated by suppression of autophagic flux drives liver malignancy.</pubmed_title><pmcid>PMC6138774</pmcid><funding_grant_id>CMRPG8F0621</funding_grant_id><funding_grant_id>CMRPG8E1651</funding_grant_id><funding_grant_id>CMRPG8C1151</funding_grant_id><funding_grant_id>CMRPG8D1033</funding_grant_id><funding_grant_id>CMRPG8D1022</funding_grant_id><funding_grant_id>CMRPG8D1023</funding_grant_id><funding_grant_id>CMRPG8D1001</funding_grant_id><funding_grant_id>CMRPG8D0561</funding_grant_id><funding_grant_id>CMRPG8D1032</funding_grant_id><funding_grant_id>CMRPG8D0751</funding_grant_id><funding_grant_id>CMRPG8F0661</funding_grant_id><funding_grant_id>CMRPG8F0662</funding_grant_id><funding_grant_id>CMRPG8A1203</funding_grant_id><pubmed_authors>Chen KD</pubmed_authors><pubmed_authors>Tsai MC</pubmed_authors><pubmed_authors>Lin CC</pubmed_authors><pubmed_authors>Huang KT</pubmed_authors><pubmed_authors>Chiu KW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tumor microenvironment mediated by suppression of autophagic flux drives liver malignancy.</name><description>The physiological role of autophagy in the catabolic process of the body involves protein synthesis and degradation in homeostasis under normal and stressed conditions. In hepatocellular carcinoma (HCC), the role of tumor microenvironment (TME) has been concerned as the main issue in fighting against this deadly malignancy. During the last decade, the crosstalk between tumor cells and their TME in HCC extensively accumulated. However, a deeper knowledge for the actual function of autophagy in this interconnection which involved in supporting tumor development, progression and chemoresistance in HCC is needed but still largely unknown. Recent studies have shown that coagulants tissue factor (TF) and factor VII (FVII) has a pathological role in promoting tumor growth by activating protease-a</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jun</publication><modification>2025-04-22T06:40:19.213Z</modification><creation>2019-03-26T23:57:15Z</creation></dates><accession>S-EPMC6138774</accession><cross_references><pubmed>30080656</pubmed><doi>10.1016/j.bj.2018.03.002</doi></cross_references></HashMap>