Role of miR‑200 family in brain metastases: A systematic review

Mol Clin Oncol. 2023 Jan 25;18(3):15. doi: 10.3892/mco.2023.2611. eCollection 2023 Mar.

Abstract

Brain metastasis (BM) represents the single most severe neurological complication of systemic cancer. The prognosis of patients with BM is poor, irrespective of the implemented treatment. The present study performed a systematic review of the literature using three online databases (PubMed, Scopus and Web of Science). Recently, a number of small RNA molecules, the microRNAs (miRNAs/miRs), have attracted increasing scientific attention. Members of the miR-200 family, which includes five miRNAs (miR-141, miR-200a, miR-200b, miR-200c and miR-429) appear to play pivotal roles in cancer initiation and metastasis. Indeed, a systematic review of the pertinent literature revealed that miR-200 family members regulate the brain metastatic cascade, particularly by modulating epithelial-to-mesenchymal transition. That holds true for the major representatives of BM, including lung and breast cancer, as well as for other less frequent secondary lesions originating from melanoma and the gastrointestinal tract. Therefore, the miRNAs may serve as potential diagnostic and/or prognostic markers, and under specific circumstances, as invaluable therapeutic targets. However, the available clinical evidence is relatively limited. A number of studies have suggested that the miR-200 family members are accurate prognostic markers of survival and resistance to chemotherapy in patients with breast cancer. Similarly, they may prove helpful in differentiating a metastatic lesion from a malignant glioma, or a hemangioblastoma from a renal cell carcinoma in patients with von Hippel Lindau syndrome, based on a cerebrospinal fluid sample. However, currently, there is no known therapeutic role for miR-200 family members in the setting of BM.

Keywords: brain metastasis; endothelial-to-mesenchymal transition; miR-200 family; pathogenesis; prognosis; therapy; zinc finger E-box-binding homeobox-1.

Grants and funding

Funding: No funding was received.