Microarray showed that lncRNA RMST was differentially expressed in cervical cancer. Further experiments were conducted to detect the expression and biological function of RMST in triple-negative breast cancer (TNBC). Microarray was used to screen the differentially expressed lncRNAs in TNBC. QRT-PCR was applied to uncover the expression of RMST in TNBC tissues. The cell viability of RMST-transfected TNBC cells were probed by CKK-8 assay and colony formation assay. TUNEL assay was conducted to test the cell apoptosis and FCM assay was exerted to detect the cell cycle. The invasion and migration ability of transfected cells were examined by transwell assay. RMST played its biological function through regulating the mRNA or protein expression in cytoplasm. CCK-8 and colony formation assay unveiled that RMST could slow down the proliferation of TNBC cells to influence the tumor progression. TUNEL results revealed that RMST could enhance cell apoptosis in TNBC. The cell cycle detected by FCM assay indicated that RMST might induce the block of G0/G1 phase thus inhibiting TNBC cell proliferation. RMST overexpression could also restrain the invasion and migration abilities of TNBC cells. RMST played a role of tumor suppressor in TNBC through inhibiting cell proliferation, invasion and migration, enhancing cell apoptosis, and regulating cell cycle.
Radiotherapy (RT) is one of most common treatments for cancer. However, overcoming the failure and side effects of RT as well as radioresistance, recurrence and metastasis remains challenging in cancer treatment. Cellular senescence (CS) is permanent arrested state of cell division induced by various factors, including exposure to ionizing radiation (IR). CS induced by IR contributes to tumour cell control and often even causes side effects in normal cells. Improvement of the therapeutic RT ratio is dependent on more cancer cell death and less normal cell damage. In addition, the biological behaviour of tumour cells after IR has also been linked to CS. This review summarizes our understanding of CS in IR, which may be beneficial for providing new insight for improving the therapeutic outcomes of RT. Contents 1. Introduction 2. IR-induced CS 3. CS and radiosensitivity 4. CS and IR side effects 5. IRIS and tumour cell biological behaviour 6. Other related mechanisms 7. Future perspectives
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