LncRNA HOTAIR enhances RCC2 to accelerate cervical cancer progression by sponging miR-331-3p

Purpose Long noncoding RNAs (lncRNAs) have been gradually regarded as influential indicators of various cancers. The present study aimed to identify the effects of lncRNA HOTAIR on cervical cancer progression. Methods RNA and protein expressions were quantified by RT-qPCR and western blot assays. Fluorescence in situ hybridization (FISH) assay was carried out to examine the intracellular location of HOTAIR. Cancer cell viability and mobility were detected by CCK-8, colony formation, transwell and wound healing assays. Binding relationships between miR-331-3p and HOTAIR/RCC2 were validated by luciferase reporter assay. Results RT-qPCR assays showed that HOTAIR levels were notably upregulated in cervical cancer tissues and cell lines. Furthermore, a fluorescence in situ hybridization (FISH) assay suggested that HOTAIR was mostly located in the cytoplasm of cancer cells, indicating a sponging function. CCK-8, colony formation, Transwell and wound-healing assays indicated that knockdown of HOTAIR in HeLa and SiHa cells significantly reduced cell growth, migration and invasion. Subsequently, miR-331-3p was proven to be the target molecule of HOTAIR. In addition, results from Pearson's correlation analysis indicated negative correlation between HOTAIR and miR-331-3p in cervical cancer tissues. HOTAIR negatively modulated miR-331-3p expression. Ultimately, the target gene of miR-331-3p was verified to be RCC2, and miR-331-3p negatively modulated RCC2 expression. In addition, analysis on clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p and RCC2. HOTAIR and RCC2 showed oncogenic functions in HeLa and SiHa cells, while miR-331-3p exerted the reverse effect. Conclusions HOTAIR plays a carcinogenic role in cervical cancer by targeting the miR-331-3p/RCC2 axis (AU)

LncRNA HOTAIR enhances RCC2 to accelerate cervical cancer progression by sponging miR-331-3p.

PURPOSE: Long noncoding RNAs (lncRNAs) have been gradually regarded as influential indicators of various cancers. The present study aimed to identify the effects of lncRNA HOTAIR on cervical cancer progression. METHODS: RNA and protein expressions were quantified by RT-qPCR and western blot assays. Fluorescence in situ hybridization (FISH) assay was carried out to examine the intracellular location of HOTAIR. Cancer cell viability and mobility were detected by CCK-8, colony formation, transwell and wound healing assays. Binding relationships between miR-331-3p and HOTAIR/RCC2 were validated by luciferase reporter assay. RESULTS: RT-qPCR assays showed that HOTAIR levels were notably upregulated in cervical cancer tissues and cell lines. Furthermore, a fluorescence in situ hybridization (FISH) assay suggested that HOTAIR was mostly located in the cytoplasm of cancer cells, indicating a sponging function. CCK-8, colony formation, Transwell and wound-healing assays indicated that knockdown of HOTAIR in HeLa and SiHa cells significantly reduced cell growth, migration and invasion. Subsequently, miR-331-3p was proven to be the target molecule of HOTAIR. In addition, results from Pearson's correlation analysis indicated negative correlation between HOTAIR and miR-331-3p in cervical cancer tissues. HOTAIR negatively modulated miR-331-3p expression. Ultimately, the target gene of miR-331-3p was verified to be RCC2, and miR-331-3p negatively modulated RCC2 expression. In addition, analysis on clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p and RCC2. HOTAIR and RCC2 showed oncogenic functions in HeLa and SiHa cells, while miR-331-3p exerted the reverse effect. CONCLUSIONS: HOTAIR plays a carcinogenic role in cervical cancer by targeting the miR-331-3p/RCC2 axis. Moreover, clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p with lncRNA HOTAIR and RCC2. These data suggested an underlying therapeutic target for cervical cancer.

KIF14 affects cell cycle arrest and cell viability in cervical cancer by regulating the p27Kip1 pathway.

BACKGROUND: Cervical cancer is a kind of malignant gynecological tumor. The first choice for treating cervical cancer is still a combination of surgery and chemoradiotherapy, but the 5-year survival rate remains poor. Therefore, researchers are trying to find new ways to diagnose and treat cervical cancer early. METHODS: The expression level of KIF14 in cells and tissues was determined via qRT-PCR. The ability of the cells to proliferate, migrate, and invade was examined using CCK-8 assay kits, colony formation assays, and Transwell chambers. The expression levels of Cyclin D1, Cyclin B1, p21, and p27 were also detected using western blot assays. RESULTS: The results suggested that p27 is a key regulatory factor in the KIF14-mediated regulation of the cell cycle. In addition, KIF14 knockdown promotes malignancy in cervical cancer cells by inhibiting p27 degradation, resulting in cell cycle arrest. CONCLUSIONS: KIF14 is an oncogene in cervical cancer, and knocking down KIF14 causes cell cycle arrest by inhibiting p27 degradation, thus affecting cell viability, proliferation, and migration. These results provide a potential therapeutic target for cervical cancer.

MicroRNA-331-3p inhibits proliferation and metastasis of ovarian cancer by targeting RCC2.

INTRODUCTION: Epithelial ovarian carcinoma (EOC) is one of the most lethal gynecologic malignancies, with a poor 5-year survival rate. Numerous studies have shown that microRNAs participate in the malignant behavior of ovarian cancer cells by directly targeting multiple oncogenes or tumor suppressor genes. MATERIAL AND METHODS: Reverse transcription-PCR was used to determine the level of miR-331-3p in EOC. Cells proliferation was measured with the Cell Counting Kit-8. Cell mobility were measured by wound-healing assay. Cell migration and invasion were measured by transwell assay. Luciferase assays were used to demonstrate that RCC2 was a directed target of miR-331-3p in EOC. Western blots were used to measure the protein expression. RESULTS: We found that the expression of microRNA-331-3p (miR-331-3p) in ovarian cancer cell lines is reduced (p < 0.01), and an increase of expression of miR-331-3p in ovarian cancer cells significantly inhibits cell proliferation (p < 0.001). Transwell and wound-healing assays showed that miR-331-3p inhibits the cell motility of ovarian cancer cells (p < 0.001). Regulator of chromosome condensation 2 (RCC2) was predicted to be a novel target for miR-331-3p. Our luciferase activity assay confirmed that RCC2 is directly targeted by miR-331-3p. RCC2 was negatively regulated by miR-331-3p (p < 0.001), and overexpression of RCC2 could restore the malignant behaviors of ovarian cancer cells, which was suppressed by miR-331-3p. CONCLUSIONS: These data indicate that miR-331-3p can inhibit proliferation, migration, and invasion of ovarian cancer cells via directly targeting RCC2. Our study provides potential therapeutic targets for the treatment of ovarian cancer.

Mechanisms of hela cell apoptosis induced by abnormal Savda Munziq total phenolics combined with chemotherapeutic agents.

OBJECTIVE: To investigate the effects of abnormal Savda Munziq (ASMq) total phenolics combined with cisplatin and docetaxel on the Hela cell growth. METHODS: In vivo cultured Hela cells were treated with cisplatin, docetaxel, total phenolics, cisplatin+total phenolics or docetaxel+total phenolics. MTT was performed to assess inhibition of cell proliferation, flow cytometry to detect apoptosis, and semi-quantitative RT-PCR to test for survivin and Bcl-2 expression. RESULTS: The total phenolics, cisplatin and docetaxel had significant inhibitory and apoptosis-promoting effects on Hela cells (P<0.05), with the early apoptotic rates of 12.8±0.70%, 18.9±3.79% and 15.8±3.8)%; the total phenolics, cisplatin and docetaxel significantly decreased the expression of Bcl-2 and survivin (all P<0.01), especially when used in combination. CONCLUSION: ASMq total phenolics, combined with cisplatin and docetaxel, could promote the apoptosis of Hela cells possibly through reducing the expression of Bcl-2 and survivin.