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RPS2 and EEF1B2 are associated with glycolysis-related malignant phenotypes in COAD
Jianbin Hou1, Yangyang Dong1, Huiyang Qian1
1Quanzhou First Hospital Affiliated to Fujian Medical University Quanzhou 362000, Fujian, China.
American Journal of Cancer Research
|July 17, 2026
Summary
Key genes RPS2 and EEF1B2 drive colon adenocarcinoma (COAD) progression by influencing lactate metabolism and glycolysis. Their knockdown inhibits cancer cell growth and migration, offering potential therapeutic targets for COAD.
Area of Science:
- Oncology
- Molecular Biology
- Metabolic Research
Background:
- Lactate metabolism reprogramming is linked to colon adenocarcinoma (COAD) progression.
- Key molecules driving this association in COAD remain largely unidentified.
Purpose of the Study:
- To identify novel genes involved in lactate metabolism and their role in COAD progression.
- To investigate the functional impact of candidate genes RPS2 and EEF1B2 on COAD cell phenotypes.
Main Methods:
- Integrated single-cell and bulk RNA sequencing data (GSE231559, TCGA-COAD).
- Applied an overlap-based screening strategy to identify candidate genes.
- Validated candidate genes using public databases, immunohistochemistry, and in vitro experiments (siRNA knockdown, co-immunoprecipitation) in HT-29 cells.
Main Results:
- Identified 14 candidate genes, prioritizing RPS2 and EEF1B2.
- RPS2 and EEF1B2 were highly expressed in COAD tumor tissues.
- Knockdown of RPS2 or EEF1B2 in HT-29 cells reduced proliferation, migration, and glycolysis-related gene expression (HK2, PFK1, PKM2, LDHA), while increasing apoptosis.
- RPS2 and EEF1B2 form a protein complex and are functionally linked in regulating malignant phenotypes.
Conclusions:
- RPS2 and EEF1B2 are significantly associated with lactate metabolism and glycolysis in COAD.
- These genes promote malignant phenotypes in COAD cells.
- RPS2 and EEF1B2 represent potential therapeutic targets for colon adenocarcinoma treatment.
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