Rpl36a, also referred to as RPL44, is a ribosomal protein. Ribosomal proteins are crucial for ribosome biogenesis and protein synthesis, processes fundamental to all living cells. The ribosome, with its complex structure, is responsible for translating mRNA into proteins, and Rpl36a is an integral part of this machinery [3,5].

In cancer research, silencing Rpl36a in colorectal cancer (CRC) cells markedly attenuated their malignant properties and tumor xenograft growth. Mechanistically, Rpl36a depletion diminished phosphorylated ERK levels, impacting the expression of c-Myc and ELK1 in the MAPK/ERK pathway, suggesting its oncogenic role in CRC [1].

In radioresistant oral squamous cell carcinoma (OSCC), knockdown of Rpl36A increased radiosensitivity via sensitizing cells to DNA damage and promoting G2/M cell cycle arrest followed by augmenting the irradiation-induced apoptosis pathway [2].

In hepatocellular carcinoma (HCC), over-expression of RPL36A led to enhanced colony formation and cell proliferation, which may have resulted from rapid cell cycling, and an antisense cDNA effectively reversed these alterations [3].

In acute myeloid leukemia (AML) cells, RPL36A expression was significantly upregulated, and its knockdown inhibited cell proliferation and induced apoptosis [4].

In conclusion, Rpl36a is important for ribosome-related functions. Model-based research, especially loss-of-function experiments in cancer cells, reveals its potential role as an oncogene in multiple cancer types, including CRC, OSCC, HCC, and AML. These findings suggest that Rpl36a could be a potential target for anticancer therapies in these disease areas.