Hmmr, also known as Hyaluronan Mediated Motility Receptor (RHAMM), is an intracellular, microtubule-associated, spindle assembly factor. It localizes protein complexes to enhance the activities of mitotic kinases like polo-like kinase 1 and Aurora kinase A, and controls dynein and kinesin motor activities. It is involved in processes such as cell migration, wound healing, and is associated with neoplastic processes [4].

In a study on hepatocellular carcinoma (HCC), an HBV-transgenic mouse model was used. HMMR was found to be transcribed by c/EBP homologous protein (CHOP) and degraded by tripartite motif containing 29 (TRIM29) after ubiquitination under endoplasmic reticulum (ER) stress. HMMR could alleviate ER stress by increasing autophagic lysosome activity, suggesting its role in the complex autophagy-ER stress relationship during HCC progression [1].

In another HCC study, an HMMR-/-liver cancer mouse model was established. HMMR knockout inhibited liver cancer growth and induced phagocytosis, revealing its role in the "don't eat me" signal dysregulation and immune evasion of HCC [2].

In prostate cancer, HMMR promoted cancer cell proliferation and metastasis through a positive feedback loop involving AURKA/mTORC2/E2F1, as demonstrated by gain-and loss-of-function approaches in vitro and in vivo [3].

In conclusion, Hmmr is a crucial regulator in multiple biological processes and diseases. Gene knockout mouse models have been instrumental in revealing its role in HCC, prostate cancer, etc. These studies suggest that Hmmr may serve as a potential therapeutic target for these cancers, highlighting its importance in understanding disease mechanisms and developing new treatment strategies.