2. Academic Validation
  3. Multi-omics data integration reveals the molecular network of dysregulation IQGAP2-mTOR promotes cell proliferation

Multi-omics data integration reveals the molecular network of dysregulation IQGAP2-mTOR promotes cell proliferation

  • Hum Cell. 2023 May 8. doi: 10.1007/s13577-023-00912-8.
Tao Chen 1 2 3,  Xijie Fan 1 2,  Guibin Li 1 2,  Yuhuan Meng 4 5 6
Affiliations

Affiliations

  • 1 Guangzhou KingMed Transformative Medicine Institute Co. Ltd., No. 10 Luoxuan 3Rd Road, Guangzhou International Biotech Island, Guangzhou, China.
  • 2 Guangzhou KingMed Diagnostics Group Co. Ltd., Guangzhou, China.
  • 3 KingMed School of Laboratory Medicine, Guangzhou Medical University, Guangzhou, China.
  • 4 Guangzhou KingMed Transformative Medicine Institute Co. Ltd., No. 10 Luoxuan 3Rd Road, Guangzhou International Biotech Island, Guangzhou, China. zb-mengyuhuan@kingmed.com.cn.
  • 5 Guangzhou KingMed Diagnostics Group Co. Ltd., Guangzhou, China. zb-mengyuhuan@kingmed.com.cn.
  • 6 KingMed School of Laboratory Medicine, Guangzhou Medical University, Guangzhou, China. zb-mengyuhuan@kingmed.com.cn.
PMID: 37154877 DOI: 10.1007/s13577-023-00912-8
Abstract

IQGAP2 as a tumor suppressor gene can influence cell proliferation in multiple tumor cell lines. However, the regulation network of cell proliferation resulting solely from the deficiency of IQGAP2 in cells was still unclear. Here, we integrated transcriptome, proteome, and phosphoproteome analyses to investigate the regulatory network of cell proliferation in IQGAP2 knockdown HaCaT and HEK293 cells. Our findings revealed that the dysregulation of the IQGAP2-mTOR molecular network led to increased cell proliferation. We demonstrated that IQGAP2 knockdown enhanced the phosphorylation levels of Akt and S6K, leading to increased cell proliferation. Additionally, we found that Akt and mTOR inhibitors partially rescued abnormal cell proliferation by reducing hyperphosphorylation. Our data suggest a potential connection between the mTOR signaling pathway and aberrant cell proliferation in IQGAP2 knockdown cells. These findings offer a new therapeutic strategy for patients with IQGAP2 deficiency.

Keywords

Cell proliferation; IQGAP2; Multi-omics; Regulation networks; mTOR.

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