{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T16:36:15Z","timestamp":1785429375048,"version":"3.56.0"},"reference-count":65,"publisher":"MDPI AG","issue":"13","license":[{"start":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T00:00:00Z","timestamp":1783382400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institute of Health, USA","award":["NIH\/NCI R01 CA245977"],"award-info":[{"award-number":["NIH\/NCI R01 CA245977"]}]},{"award":["NIH\/NCI R01 CA245977"],"award-info":[{"award-number":["NIH\/NCI R01 CA245977"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"name":"VA Merit Review","award":["I01 BX005066"],"award-info":[{"award-number":["I01 BX005066"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Stress MAPKp38\u03b3 (MAPK12) has established roles in promoting tumorigenesis; however, the mechanisms involved remain largely unclear. This paper will review recently published and unpublished studies of p38\u03b3 in programming immune evasion in breast cancer, pancreatic cancer, and colon cancer to promote tumorigenesis. First, we show that p38\u03b3 is an oncogene that transforms breast epithelial cells into triple-negative breast cancer (TNBC), is required for breast tumorigenesis in mice, and activates tumor-suppressive environments via a positive feedback signaling loop. Moreover, we show that epithelial p38\u03b3 is required for KRAS-oncogene-induced pancreatic cancer in two genetic murine models (KPC and KTC) by activating glycolytic pathways to provide metabolic support for cancer cells and by increasing chemokine CXCL5-dependent fibrosis and immune cell infiltrations. Lastly, we will delineate how p38\u03b3 is activated by the main risk factors for colon cancer and serves as a key integrator of oncogenic and inflammatory signaling to promote tumorigenesis by increasing Wnt proliferative signaling and programming immune evasion. These results indicate that p38\u03b3 MAPK can integrate common risk factors for colon cancer and amplify oncogenic signaling by phosphorylating its substrate, \u03b2-catenin, increasing transcription of Wnt and the chemokine CXCL13, and promoting PD-L1 expression. In each of these tumor models, we will present evidence supporting our hypothesis, followed by additional experiments for verification. Our studies suggest that targeting p38\u03b3 may be an innovative approach in cancer therapeutic intervention.<\/jats:p>","DOI":"10.3390\/cells15131226","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T08:04:49Z","timestamp":1783411489000},"page":"1226","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["P38\u03b3 Promotes Tumorigenesis Through Activating Immune Evasion"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4951-1277","authenticated-orcid":false,"given":"Naveenkumar","family":"Chandrashekar","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao-Mei","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA"},{"name":"Research Service, Clement J. 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