Targeting YES1 enhances the efficacy of chemotherapy, targeted therapy and onco-immunotherapy

Area of Science:

• Oncology
• Molecular Biology
• Drug Discovery

Background:

• YES1 (Yamaguchi sarcoma virus homolog 1), a SRC family tyrosine kinase, is frequently altered in solid tumors.
• YES1 alterations promote tumor progression, metastasis, and resistance to cancer therapies through bypass pathways.
• Existing SRC family kinase inhibitors face limitations due to toxicity and lack of selectivity.

Purpose of the Study:

• To summarize the mechanisms by which YES1 drives tumor progression and resistance.
• To review the potential of YES1-selective inhibitors and combination therapies.
• To discuss novel therapeutic strategies targeting YES1.

Main Methods:

• Literature review and synthesis of existing research on YES1.
• Analysis of YES1's role in oncogenic pathways (e.g., YES1-YAP1, EGFR-YES1 crosstalk).
• Exploration of YES1's function in the tumor microenvironment and synthetic lethality.

Main Results:

• YES1 plays a critical role in multiple aspects of tumor biology, including growth and metastasis.
• YES1 contributes significantly to therapeutic resistance.
• YES1-selective inhibitors and combination therapies demonstrate synergistic anti-tumor effects.

Conclusions:

• Targeting YES1 is a viable strategy to overcome drug resistance and suppress tumor growth.
• Combinational approaches involving YES1 inhibitors show significant promise for cancer treatment.
• Further investigation into YES1-targeted therapies could lead to improved patient outcomes and quality of life.