Abstract
Emerging studies have clarified the critical role of LncRNA MALAT1 in various pathological progressions. Here, we identified its positive relationship with cervical carcinoma proliferation. Cervical carcinoma has been considered as one of the most malignant tumors among female. Thus, our study was designed to investigate the underlying mechanism of LncRNA MALAT1 on cervical tumor cell proliferation. We observed that miR-124 was the potential target of LncRNA MALAT1 in cervical tumor cell lines (Hela, C-33A, Caski, and SiHa), the expression level of which is negatively correlated with LncRNA MALAT1 in cervical tumor cells, tissues of cervical patients, and mice. Gain- or loss-of-function analyses in cervical tumor cells have further verified the regulatory role of MALAT1 on miR-124. Additionally, the proliferation of cervical carcinoma was inhibited by miR-124 overexpression, whereas it was blocked by LV-MALAT1 transfection. In vivo assays, overexpression of miR-124, or knockdown of MALAT1 exhibited beneficial effects on tumor weight, size, and volume, together with elevating the survival rate, tightly related with the progression of cervical cancer. In conclusion, LncRNA MALAT1 disabled the effects of miR-124 as an inhibitory sponge, accelerating the progression of cervical carcinoma.
Highlights
Cervical carcinoma is one of the most life-threatening neoplasms among female, which is characterized as low survival rate at the advanced stage [1]
Conservation is the most important property for LncRNAs to perform its function. us, in our present study, we aimed to investigate the underlying mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in the progression of cervical carcinoma, which is characterized as good conservation
We further explored its potential downstream target, miR-124. e expression levels of miR-124 were downregulated in carcinoma tissues and cervical tumor cells compared with paracarcinoma tissues and End1/E6E cells (Figures 1(c) and 1(e)). ese results suggested a negative relationship between LncRNA MALAT1 and miR-124. us, we subsequently examined LncRNA MALAT1 and miR-124 by real-time PCR in cervical carcinoma tissue compared with its paracarcinoma tissue, as well as in mice tumor tissues. e results showed that the expression levels of LncRNA MALAT1 and miR124 were negatively related in the progression of cervical carcinoma, nor in normal conditions (Figures 1(f )–1(h) and Table 2). us, we concluded that the LncRNA MALAT1 expression level is negatively related to miR-124, implying their regulatory relationship in the progression of cervical carcinoma
Summary
Cervical carcinoma is one of the most life-threatening neoplasms among female, which is characterized as low survival rate at the advanced stage [1]. With the development of precision therapy, research studies on potential molecular targets were demonstrated to play an important role in malignant diseases. The key role of LncRNAs on cervical carcinoma has been addressed [7,8,9,10], including PTCSC3, NEAT1, UCA1, and MALAT1. Among these LncRNAs, MALAT1 has been commonly considered as a promising therapeutical target due to its well-conserved property between species [11, 12]. Researchers have clarified the regulatory effects of MALAT1 on breast cancer via inactivating prometastatic transcription factor TEAD [14], as well as promoting epithelial ovarian cancer by the PI3KAKT pathway [15]. Studies on cervical carcinoma are required to be further improved, and the underlying mechanism remains unclear
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