{"title":"Sini decoction-polysaccharide compound regulates proliferation, apoptosis, and glycolysis of liver cancer cells through PHLDA2/ANXA2.","authors":"Churan Shen, Peipei Huang, Wuji Xie, Xing Ni, Jingdong Gao","doi":"10.21037/tcr-24-1625","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Sini decoction (SND), a popular formula from traditional Chinese medicine (TCM), plays a critical role in the treatment of liver disease. Its protective effect for the heart against cardiovascular diseases is well documented. However, its effects and pharmacological mechanisms for the liver remain unclear. This study aimed to clarify the effect and mechanism of the SND-polysaccharide compound (SNDPC) on hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>Different genes affected by SNDPC in HCC were analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Databases including Multi-Experiment Matrix (MEM), HCCDB, LinkedOmics, and Gene Expression Profiling Interactive Analysis (GEPIA) were used to determine the correlation between <i>PHLDA2</i> and <i>ANXA2</i>. Cell proliferation and viability were identified using Cell Counting Kit-8 (CCK-8). Cell apoptosis was estimated using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and Western blotting. Glycolysis was determined by measuring glucose uptake, lactate concentration, extracellular acidification rate (ECAR), and the expressions of LHDA, HK2, and PKM2. The binding between PHLDA2 and ANXA2 was identified by coimmunoprecipitation.</p><p><strong>Results: </strong>SNDPC significantly weakened cell proliferation, facilitated cell apoptosis, and suppressed glycolysis by reducing glucose uptake, lactate concentration, ECAR, and the expressions of LDHA, HK2, and PKM2 in HCC cells. Furthermore, PHLDA2 was predicted to bind to ANXA2, which was confirmed by coimmunoprecipitation. SNDPC reduced the expressions of PHLDA2 and ANXA2 in HCCLM3 cells, and PHLDA2 silencing decreased the proliferation of cells, promoted cell apoptosis, and inhibited glycolysis of HCCLM3 cells while reversing the overexpression of PHLDA2.</p><p><strong>Conclusions: </strong>SNDPC suppressed proliferation and glycolysis while accelerating the apoptosis of HCC cells through PHLDA2/ANXA2.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"13 10","pages":"5574-5587"},"PeriodicalIF":1.5000,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11543045/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/tcr-24-1625","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/29 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Sini decoction (SND), a popular formula from traditional Chinese medicine (TCM), plays a critical role in the treatment of liver disease. Its protective effect for the heart against cardiovascular diseases is well documented. However, its effects and pharmacological mechanisms for the liver remain unclear. This study aimed to clarify the effect and mechanism of the SND-polysaccharide compound (SNDPC) on hepatocellular carcinoma (HCC).
Methods: Different genes affected by SNDPC in HCC were analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Databases including Multi-Experiment Matrix (MEM), HCCDB, LinkedOmics, and Gene Expression Profiling Interactive Analysis (GEPIA) were used to determine the correlation between PHLDA2 and ANXA2. Cell proliferation and viability were identified using Cell Counting Kit-8 (CCK-8). Cell apoptosis was estimated using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and Western blotting. Glycolysis was determined by measuring glucose uptake, lactate concentration, extracellular acidification rate (ECAR), and the expressions of LHDA, HK2, and PKM2. The binding between PHLDA2 and ANXA2 was identified by coimmunoprecipitation.
Results: SNDPC significantly weakened cell proliferation, facilitated cell apoptosis, and suppressed glycolysis by reducing glucose uptake, lactate concentration, ECAR, and the expressions of LDHA, HK2, and PKM2 in HCC cells. Furthermore, PHLDA2 was predicted to bind to ANXA2, which was confirmed by coimmunoprecipitation. SNDPC reduced the expressions of PHLDA2 and ANXA2 in HCCLM3 cells, and PHLDA2 silencing decreased the proliferation of cells, promoted cell apoptosis, and inhibited glycolysis of HCCLM3 cells while reversing the overexpression of PHLDA2.
Conclusions: SNDPC suppressed proliferation and glycolysis while accelerating the apoptosis of HCC cells through PHLDA2/ANXA2.
期刊介绍：
Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.
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