OCIAD2 Promotes Cancer Progression via Metabolic Reprogramming in Lung Adenocarcinoma

TL;DR

This study identifies OCIAD2 as a protein linked to lung cancer progression by altering cellular metabolism.

Contribution

The study reveals OCIAD2's role in promoting lung adenocarcinoma through metabolic reprogramming.

Findings

OCIAD2 is highly expressed in 95.5% of lung adenocarcinoma patients and correlates with worse survival.

Silencing OCIAD2 reduces cancer cell migration, invasion, and colony formation.

OCIAD2 impairs oxidative phosphorylation and shifts metabolism toward glycolysis.

Abstract

Given the limited proteomic insights and high incidence
of lung
adenocarcinoma, further investigation of uncharacterized proteins
in cancer progression remains crucial. In this study, a poorly characterized
protein, OCIA domain-containing 2 (OCIAD2), encoded by chromosome
4 was identified as being upregulated in lung adenocarcinoma from
our previous proteogenomics data using the Taiwan Cancer Moonshot
cohort. OCIAD2 was highly expressed in tumor tissues in 95.5% of lung
adenocarcinoma patients in our cohort, with elevated expression correlating
with worse survival. Functional studies revealed that the silencing
of the OCIAD2 decreased cell migration, invasion, and colony-forming
abilities. Gene Set Enrichment Analysis (GSEA) indicated the involvement
of OCIAD2 in oxidative phosphorylation (OXPHOS). Subsequently, mitochondrial
metabolic assay demonstrated that OCIAD2 impairs OXPHOS function,
accompanied by a metabolic shift toward glycolysis. These findings
suggest that OCIAD2 promotes cancer progression through metabolic
reprogramming, highlighting the role of OCIAD2 as a potential biomarker
and therapeutic target for lung adenocarcinoma.

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