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Expression profile and bioinformatics analysis of COMMD10 in BALB/C mice and human

Yao Fan1, Longshan Zhang1, Yaling Sun1

  • 1Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.

Cancer Gene Therapy
|February 22, 2019
PubMed

Insights

COMMD10 protein suppresses tumor growth by inhibiting the nuclear factor-kappaB (NF-kappaB) pathway. This study maps its expression in normal and tumor tissues, revealing its potential role in renal clear cell carcinoma prognosis and chemotherapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • COMMD10 protein is known to inhibit the nuclear factor-kappaB (NF-kappaB) pathway, suppressing colorectal cancer invasion and metastasis.
  • Understanding COMMD10's expression patterns and biological distribution is crucial for elucidating its role in various cancers.

Purpose of the Study:

  • To investigate the expression profile and tissue distribution of COMMD10 in human normal and tumor tissues.
  • To explore the potential mechanisms and biological functions of COMMD10 and its interacting genes.

Main Methods:

  • Analysis of COMMD10 expression in mouse and human tissues via immunohistochemistry.
  • Utilized TCGA database for expression profiling and STRING database for identifying interacting genes.
  • Predicted microRNA targets using miRDB, miRWalk, and TargetScan.
  • Performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.

Main Results:

  • COMMD10 mRNA expression was highest in lung and spleen, lowest in heart and brain. Immunohistochemistry showed varied expression, mainly cytoplasmic, with nuclear/cytoplasmic localization in liver cells.
  • Positive cytoplasmic staining for COMMD10 was observed in most tumor tissues, excluding specific types like lung adenocarcinoma and cervical cancer.
  • Increased COMMD10 expression correlated with longer survival in renal clear cell carcinoma patients.
  • Identified 41 interacting genes and hsa-miR-590-3p as a potential regulator.
  • GO and KEGG analyses implicated COMMD10 in ubiquitin ligase complexes, copper ion transport, transcription, translation, NF-kappaB regulation, renal cell carcinoma, and HIF-1 signaling.

Conclusions:

  • COMMD10 exhibits diverse tissue distribution and expression patterns in normal and cancerous tissues.
  • COMMD10 may act as a tumor suppressor in renal clear cell carcinoma via the miR-590-3p-COMMD10-Cul2-RBX1-NF-κB/HIF/NRF2 pathway.
  • COMMD10 influences chemotherapy resistance in various tumors, suggesting therapeutic potential.

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