# 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.

## Key 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.