The long non-coding RNA, urothelial cancer-associated 1 (UCA1) is an important regulator in several tumors. However, to the best of our knowledge, the clinical roles of UCA1 in cervical cancer remain unclear. Thus, the present study aimed to investigate the function and mechanism of UCA1 in cervical cancer. Reverse transcription-quantitative PCR analysis was performed to detect UCA1 and microRNA (miR)-299-3p expression in cervical cancer tissues and cell lines. The Cell Counting Kit-8 and Transwell assays were performed to assess cell proliferation and invasion, respectively. Furthermore, the dual-luciferase reporter assay was performed to confirm the association between UCA1 and miR-299-3p. Rescue experiments were performed to determine the mechanism of the UCA1/miR-299-3p axis. The results demonstrated that UCA1 expression was upregulated in cervical cancer tissues and cell lines. Furthermore, overexpression of UCA1 enhanced the proliferation and invasion of cervical cancer cells, the effects of which were reversed following UCA1 knockdown. Notably, UCA1 interacted with miR-299-3p and negatively regulated miR-299-3p expression. In addition, miR-299-3p expression was downregulated in cervical cancer tissues and cell lines. Overexpression of miR-299-3p suppressed the proliferation and invasion of cervical cancer cells, reversing the effects of UCA1 knockdown on cervical cancer cell proliferation. Taken together, the results of the present study suggest that UCA1 promotes cell proliferation and invasion by regulating miR-299-3p expression in cervical cancer.
Background Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear. Objective The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer. Methods The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms. Results SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells. Conclusions SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.
Ovarian cancer (OC) is one of known gynecologic malignant tumors, posing a serious threat to women’s life, and this disorder is often not diagnosed until it’s more advanced. This study aimed to identify the efficacy of polydopamine (PDA) nanoparticles loaded with EPB41L4A-AS2 (EPB) on OC. PDA nanoparticles-loaded EPB (PDA-EPB) were prepared, and OC cells were administrated with 10 μmol/LPDA-EPB nanoparticles or 10 μmol LHBSS buffer (control group). Untreated cells were taken as control group, and CCK-8 assay was conducted 24 h after treatments, to detect cell proliferation, while Transwell assay was used to detect invasion. Apoptosis was evaluated by flow cytometry along with analysis of Bax, Bcl-2, and caspase-3 apoptosis genes expression as well as the expression of Erk1/2, JNK, and p38 proteins. PDA-EPB nanomaterials presented uniform nanoparticle size of 100 nm and hydrated particle size of 190 nm. Treatment with composite nanoparticles decreased proliferation of OC cells over time. The increased concentration of nanoparticles occurred with decreased proliferation activity and 10 μmol/L was the best intervention concentration. Besides, PDA-EPB nanomaterials resulted in decreased number of invaded and migrated cells (41.03±3.95%) and increased apoptosis rate (33.59±3.23%), compared with the other two groups. The apoptosis ability was significantly higher, P < 0.05. Meanwhile, in the presence of PDA-EPB nanoparticles, the experimental group presented low expressions of Bad (1.96 ±0.23), Bcl-2 (1.56± 0.34), Caspase-3 (2.89± 0.28) and (0.98 ±0.39), JNK (0.53±0.31), and p38 (0.79±0.26). PDA-EPB nanoparticles therefore decreased cell proliferation and induced apoptosis through specifically binding to the MAPK signaling pathway to activate the expression of Erk1/2, JNK, and p38 in OC.
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