Rasl11a, a member of a novel small monomeric GTPase gene family, has been implicated in various biological processes. It is involved in the regulation of pre-ribosomal RNA (pre-rRNA) synthesis, existing in stable complexes with the RNA polymerase I-specific transcription factor UBF in the nucleolus and marking active rDNA repeats [4]. It may act in concert with UBF to facilitate transcription by RNA polymerase I.

In cancer research, a single point mutation in the 5' untranslated region of Rasl11a significantly contributes to tumor regression in Tasmanian devils, with its expression in regressed tumors but silencing in non-regressed ones, similar to its down-regulation in human cancers [1]. In glioblastoma, higher Rasl11a expression correlates with poor clinical outcomes and it reduces radiosensitivity by enhancing STAT3 phosphorylation [2]. In prostate tumors, it is down-regulated, suggesting a potential tumor suppressor role [3]. Also, in colorectal cancer, it escapes copy number-induced overexpression and its overexpression affects cell proliferation, migration, and anchorage-independent growth [6]. In lymphoma, it was screened as a potential radiotherapy-resistant gene [5].

In conclusion, Rasl11a plays diverse and significant roles in biological processes such as rRNA synthesis and in various disease conditions, especially cancer. Studies on Rasl11a, including those using genetic models in different species, have provided insights into its functions, highlighting its potential as a therapeutic target in cancer treatment.