Long non-coding RNA Linc00657 up-regulates Skp2 to promote the progression of cervical cancer through lipid reprogramming and regulation of immune microenvironment.

More and more evidence shows that long non-coding RNA (lncRNA) plays an important role in the biological behavior of many kinds of malignant tumors, but the specific function of lncRNA Linc00657 in cervical cancer is still unknown. The purpose of this study is to explore the effect of Linc00657 on the malignant progression of cervical cancer and its potential mechanism. In two kinds of cervical cancer cell lines and normal cervical epithelial cells, qRT-PCR showed increased expression of Linc00657 in cervical cancer cells. Through MTT, clone formation test, flow cytometry, wound healing test and Transwell test, it has been found that overexpression of Linc00657 could promote the proliferation,migration and invasion of cervical cancer cells，and inhibit apoptosis. Through the StarBase database, it was found that there may be a mutual regulatory relationship between Linc00657 and Skp2, and Skp2 may be the downstream target of Linc00657. QRT-PCR detection confirmed that the expression of Skp2 was increased in cervical cancer cells with overexpression of Linc00657. TIMER2 database found that Skp2 was associated with lipid metabolic enzymes and immune cell infiltration. It was found that Linc00657 knockdown inhibited tumor growth and metastasis and inhibited the expression of Skp2 in vivo. In short, our research shows that Linc00657 has carcinogenic properties in cervical cancer, and LINC00657 promotes the occurrence of cervical cancer by up-regulating the expression of Skp2. We predict that Linc00657/mir30s/Skp2 axis plays a role in the malignant progression of cervical cancer. In addition, Skp2 may participate in cancer immune response and promote lymph node metastasis of cervical cancer through lipid reprogramming. These findings also provide promising targets for the diagnosis and treatment of cervical cancer.

Expression and correlation analysis of Skp2 and CBX7 in cervical cancer.

AIMS: S-phase kinase-associated protein 2 (Skp2) oncoprotein is overexpressed in a variety of cancer tissues and promotes the malignant development of cancer. The expression levels of chromobox homolog 7 (CBX7) protein are varied among different types of cancer tissues, but its role in cervical cancer is not clear. We aimed to examine the expression and clinical significance of Skp2 and CBX7 proteins as well as their correlations in cervical cancer. METHODS: Immunohistochemistry was used to detect the expression of Skp2 and CBX7 proteins in the cancerous tissues and adjacent tissues of 64 patients with cervical cancer. Relevant clinicopathological data of these patients were collected, compared and analysed for the correlations. RESULTS: The expression of Skp2 protein in cervical cancer (87.5%) was higher than that in paracancerous tissues (14.1%), and the expression was positively correlated with clinical stage, malignant degree, lymphatic metastasis, vascular invasion and interstitial invasion. The expression of CBX7 protein in cervical cancer (48.4%) was lower than that in paracancerous tissues (96.8%), and the expression was negatively correlated with clinical stage, malignant degree, interstitial invasion, vascular invasion and lymphatic metastasis. The expression of Skp2 protein and CBX7 protein in cervical cancer tissues and adjacent tissues was negatively correlated. The expression of Skp2 and CBX7 proteins was closely related to the clinicopathological features of cervical cancer. CONCLUSIONS: CBX7 may play the role of a tumour suppressor gene in cervical cancer and provide reference value for the diagnosis and new targeted treatment of cervical cancer.

LncRNA SCAMP1 disrupts the balance between miR-26a-5p and ZEB2 to promote osteosarcoma cell viability and invasion.

Osteosarcoma often occurs in children and adolescents and affects their health. The survival rate of osteosarcoma patients is unsatisfactory due to the lack of early detection and metastasis development and drug resistance. Hence, dissection of molecular insight into osteosarcoma initiation and progression is pivotal to provide the new therapeutic strategy. In recent years, long noncoding RNAs (lncRNAs) have burst into stage in osteosarcoma development and malignant behaviors. LncRNA SCAMP1 has been discovered to play an essential role in carcinogenesis and progression. However, the mechanisms of lncRNA SCAMP1-involved tumorigenesis have not been reported in human osteosarcoma. In this study, we utilized multiple cellular biological approaches to determine the function of lncRNA SCAMP1 in osteosarcoma cells. Moreover, we performed several molecular biological approaches to define the mechanism by which lncRNA SCAMP1 regulated cell viability and invasion in osteosarcoma. We dissected that lncRNA SCAMP1 promoted progression of osteosarcoma via modulation of miR-26a-5p/ZEB2 axis. In conclusion, targeting lncRNA SCAMP1 and its downstream targets, miR-26a-5p and ZEB2, might be a useful approach for osteosarcoma therapy.