A promising new strategy for cancer therapy is to target the autophagic pathway. However, comprehensive characterization of autophagy genes and their clinical relevance in cancer is still lacking. Here, we systematically characterized alterations of autophagy genes in multiple cancer lines by analyzing data from The Cancer Genome Atlas and CellMiner database. Interactions between autophagy genes and clinically actionable genes (CAGs) were identified by analyzing co-expression, protein-protein interactions (PPIs) and transcription factor (TF) data. A key subnetwork was identified that included 18 autophagy genes and 22 CAGs linked by 28 PPI pairs and 1 TF-target pair, which was EGFR targeted by RARA. Alterations in the expression of autophagy genes were associated with patient survival in multiple cancer types. RARA and EGFR were associated with worse survival in colorectal cancer patients. The regulatory role of EGFR in 5-FU resistance was validated in colon cancer cells in vivo and in vitro. EGFR contributed to 5-FU resistance in colon cancer cells through autophagy induction, and EGFR overexpression in 5-FU resistant colon cancer was regulated by RARA. The present study provides a comprehensive analysis of autophagy in different cancer cell lines and highlights the potential clinical utility of targeting autophagy genes.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6977699 | PMC |
| http://dx.doi.org/10.18632/aging.102607 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Stress granules sequester autophagy proteins to facilitate plant recovery from heat stress.
Nat Commun
December 2024
Guangdong Provincial Key Laboratory of Biotechnology for Plant Development, School of Life Sciences, South China Normal University, Guangzhou, China.
The autophagy pathway regulates the degradation of misfolded proteins caused by heat stress (HS) in the cytoplasm, thereby maintaining cellular homeostasis. Although previous studies have established that autophagy (ATG) genes are transcriptionally upregulated in response to HS, the precise regulation of ATG proteins at the subcellular level remains poorly understood. In this study, we provide compelling evidence for the translocation of key autophagy components, including the ATG1/ATG13 kinase complex (ATG1a, ATG13a), PI3K complex (ATG6, VPS34), and ATG8-PE system (ATG5), to HS-induced stress granules (SGs) in Arabidopsis thaliana.
View Article and Find Full Text PDFTranscriptome analysis reveals the genetic basis underlying the formation and seasonal changes of nuptial pads in Rana chensinensis.
BMC Genomics
December 2024
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, 152 Luoyulu, Hongshan District, Wuhan, 430079, China.
Background: Nuptial pads, a typical sexually dimorphic trait in anurans, are located on the first digit of the male forelimb in Rana chensinensis and exhibit morphological changes synchronized with breeding cycles. However, the genetic mechanisms underlying its formation and seasonal changes remain poorly understood.
Results: To identify genes and biological processes associated with the development and seasonal variations of nuptial pads, we conducted a comprehensive transcriptome analysis on nuptial pads and hind toe skin across both sexes at different breeding periods in R.
Deciphering Glioblastoma Pathogenesis: Insights from Mitophagy Dysregulation and SNX7 as a Therapeutic Target.
Brain Res Bull
December 2024
Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, Fujian, China; Department of Neurosurgery, Binhai Branch of National Regional Medical Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, Fujian, China; Fujian Provincial Institutes of Brain Disorders and Brain Sciences, First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, Fujian, China. Electronic address:
Background: Glioblastoma is a highly aggressive and invasive brain tumor with an extremely poor prognosis. The aims of the present study are to investigate the pathogenesis of glioblastoma and identify potential therapeutic targets.
Methods: We performed a systematic analysis of gene expression data from multiple datasets, including GEO and TCGA, to identify hub genes and pathways associated with glioblastoma progression.
Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy.
Oncol Res
December 2024
Department of Respiratory and Critical Care Medicine, Nanping First Hospital Affiliated to Fujian Medical University, Nanping, 353006, China.
Background: Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear.
Methods: LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth.
Insights into targeting LKB1 in tumorigenesis.
Genes Dis
March 2025
The Mary & John Knight Translational Ovarian Cancer Research Unit, London Regional Cancer Program, London, ON N6A 4L6, Canada.
Genetic alterations to serine-threonine kinase 11 () have been implicated in Peutz-Jeghers syndrome and tumorigenesis. Further exploration of the context-specific roles of liver kinase B1 (LKB1; encoded by ) observed that it regulates AMP-activated protein kinase (AMPK) and AMPK-related kinases. Given that both migration and proliferation are enhanced with the loss of LKB1 activity combined with the prevalence of genetic alterations in cancer biopsies, LKB1 was marked as a tumor suppressor.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!