Related Experiment Video
Updated: Sep 8, 2025

Multidimensional Coculture System to Model Lung Squamous Carcinoma Progression
Published on: March 17, 2020
OCIAD2 Promotes Cancer Progression via Metabolic Reprogramming in Lung Adenocarcinoma.
Yi-Hui Huang1,2, Wen-Hsin Chang3, Chi-Ya Shen1
1Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei 10048, Taiwan.
Lung adenocarcinoma progression is linked to the protein OCIAD2. This study found OCIAD2 promotes cancer growth by altering cell metabolism, suggesting it as a potential therapeutic target.
Area of Science:
- Molecular Biology
- Cancer Research
- Biochemistry
Background:
- Lung adenocarcinoma has a high incidence and limited proteomic understanding.
- Uncharacterized proteins are critical for understanding cancer progression.
- OCIAD2 (OCIA domain-containing 2) was identified as upregulated in lung adenocarcinoma.
Purpose of the Study:
- To investigate the role of OCIAD2 in lung adenocarcinoma progression.
- To explore OCIAD2's impact on cell migration, invasion, and colony formation.
- To determine OCIAD2's involvement in cellular metabolism and its effect on oxidative phosphorylation.
Main Methods:
- Proteogenomic analysis of the Taiwan Cancer Moonshot cohort.
- Gene silencing of OCIAD2 in lung adenocarcinoma cells.
- Gene Set Enrichment Analysis (GSEA).
- Mitochondrial metabolic assays.
Main Results:
- OCIAD2 was highly expressed in 95.5% of lung adenocarcinoma tumor tissues.
- Elevated OCIAD2 expression correlated with worse patient survival.
- OCIAD2 silencing reduced cell migration, invasion, and colony formation.
- OCIAD2 impairs oxidative phosphorylation (OXPHOS) and promotes glycolysis.
Conclusions:
- OCIAD2 promotes lung adenocarcinoma progression via metabolic reprogramming.
- OCIAD2 functions as a potential biomarker for lung adenocarcinoma.
- OCIAD2 represents a potential therapeutic target for lung adenocarcinoma.
More Related Videos
09:38Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
07:39The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Cancer Cell Migration through Invadopodia
Cancer Stem Cells and Tumor Maintenance
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Targeted Cancer Therapies
There are several types of targeted therapies against...