Guowen Ren
Shenzhen, 518055, China
Last Updated: 09/26/2026
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Found 14 publications
ARID1A deficiency activates OSM-STAT3 axis in endometrial cancer, creating vulnerability to JAK/STAT3 inhibition.
Journal: International journal of biological sciences
Published: November 28, 2025
DNA methyltransferase inhibition is a therapeutic vulnerability in VHL-deficient renal cell carcinoma cells.
Journal: Experimental & molecular medicine
Published: September 03, 2025
PTEN-deficient, chromosomal instability colorectal cancer is hypersensitive to STAT3 inhibition.
Journal: International journal of biological sciences
Published: January 28, 2025
Microtubule dynamics is a therapeutic vulnerability in VHL-deficient renal cell carcinoma.
Journal: International journal of biological sciences
Published: December 30, 2024
Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.
Journal: Experimental & molecular medicine
Published: May 14, 2024
BET inhibition induces synthetic lethality in PTEN deficient colorectal cancers via dual action on p21CIP1/WAF1.
Journal: International journal of biological sciences
Published: November 03, 2023
MDM2 inhibition is synthetic lethal with PTEN loss in colorectal cancer cells via the p53-dependent mechanism.
Journal: International journal of biological sciences
Published: January 11, 2023
ER translocon inhibitor ipomoeassin F inhibits triple-negative breast cancer growth via blocking ER molecular chaperones.
Journal: International journal of biological sciences
Published: December 20, 2022
Aurora kinase A inhibition induces synthetic lethality in SMAD4-deficient colorectal cancer cells via spindle assembly checkpoint activation.
Journal: Oncogene
Published: November 08, 2021
Natural products targeting cancer cell dependency.
Journal: The Journal of antibiotics
Published: April 29, 2021
Aurora kinase A, a synthetic lethal target for precision cancer medicine.
Journal: Experimental & molecular medicine
Published: February 05, 2021
Bromodomain and extra-terminal motif (BET) inhibition is synthetic lethal with loss of SMAD4 in colorectal cancer cells via restoring the loss of MYC repression.
Journal: Oncogene
Published: August 13, 2020
Last Updated: 09/26/2026