Overall, our research showed promising potential for new treatment strategies based on epigenetic regulation targeting MALAT1, which will not only coordinate with the patient's immune system, but also eliminate OS in conjunction with chemotherapy.
The functional experiments show that a decreased MALAT1 could remarkably inhibit osteosarcoma cell metastasis and proliferation but induce cell cycle arrest, indicating that MALAT1 functioned as an oncogene in osteosarcoma.
Metastasis‑associated lung adenocarcinoma transcript 1 (MALAT‑1) has been reported to upregulated and epigenetically regulate the metastasis in osteosarcoma; however, the regulatory mechanisms of MALAT‑1 expression remain unclear.
Suppression of FOXO1, identified as a regulatory transcriptional factor of MALAT1, was shown to be able to slow down both proliferation and metastases in OS cells, suggesting that targeting FOXO1 can be useful in the therapy of patients with OS.
Recently, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a lncRNA, has been discovered to be closely related to OS progression and hypoxia responses which are associated with angiogenesis.
Our results demonstrated the clinical prognostic significance and roles of MALAT1 in osteosarcoma, and suggested that MALAT1 may be considered as a prognostic biomarker and therapeutic target for osteosarcoma.
17β-estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner.