HMMR is a novel prognostic marker and a potential therapeutic target for colon cancer.

The hyaluronan-mediated motility receptor (HMMR) is a critical regulator of tumor progression, yet its specific role in colon cancer remains poorly understood. This study aims to better understand the molecular mechanism of HMMR in colon cancer progression. We modulated HMMR expression (overexpression and knockdown) in colon cancer cells and assessed its impact on proliferation, migration, and chemoresistance using in vitroassays (CCK-8, colony formation, transwell migration, EdU incorporation) and in vivo xenograft models. HMMR expression at the mRNA and protein levels was quantified via real-time polymerase chain reaction and Western blotting, while apoptosis and cell cycle were evaluated by flow cytometry. Clinical colon cancer specimens were analyzed by immunohistochemistry, and transcriptome sequencing was performed to identify downstream effectors and signaling pathways.Our findings demonstrate that HMMR is significantly upregulated in colon cancer tissues and cell lines, correlating with poor patient prognosis. Functional studies revealed that HMMR overexpression promotes cell proliferation, migration, and chemoresistance, whereas its knockdown exerts inhibitory effects. Notably, UTP20 small subunit processome component (UTP20) was identified as a key downstream effector of HMMR, with its expression elevated upon HMMR overexpression. UTP20 overexpression promoted the proliferation and migration of colon cancer cells. Moreover, it was found that HMMR can significantly enhance proliferation and migration in colon cancer cells by regulating the mTOR signaling pathway. In conclusion, HMMR plays an important role in promoting progression in colon cancer cells and is expected to be a potential therapeutic target.