Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) sponges microRNA-124-3p to up-regulate phosphodiesterase 4B (PDE4B) to accelerate the progression of Parkinson's disease.

Reportedly, long non-coding RNA (lncRNA) are crucial modulators in neurodegenerative diseases. Herein, we investigated the role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in Parkinson's disease (PD). In-vitro PD model was established based on SH-SY5Y cells treated with 1-methyl-4-phenylpyridinium (MPP+). NEAT1, microRNA (miR) -124-3p and phosphodiesterase 4B (PDE4B) expression levels were examined by qRT-PCR. CCK-8 assay and LDH release assay were adopted to delve into the cell viability and cytotoxicity, respectively. Besides, western blot was utilized to determine mTOR, p-mTOR and PDE4B expression levels. ELISA was executed to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß) and interleukin 6 (IL-6). Dual-luciferase reporter assay and RIP assay were used to probe the relationship between miR-124-3p and NEAT1 or PDE4B. We demonstrated that, in SH-SY5Y cells treated with MPP+, NEAT1 and PDE4B expression levels were raised, while miR-124-3p expression was repressed; NEAT1 depletion or miR-124-3p overexpression increased the cell viability and suppressed cell injury. Besides, miR-124-3p was confirmed as the direct target of NEAT1, and its down-regulation counteracted the impact of NEAT1 depletion on SH-SY5Y cells. PDE4B was as the downstream target of miR-124-3p, and its overexpression weakens the impact of miR-124-3p on SH-SY5Y cells. Additionally, NEAT1 decoyed miR-124-3p to modulate PDE4B expression. Collectively, in MPP+-induced SH-SY5Y cells, NEAT1 depletion increases cell viability, represses cytotoxicity and reduces inflammatory response by regulating miR-124-3p and PDE4B expression levels, suggesting that NEAT1 may be a promising target for treating PD.

Upregulation of circ_0000142 promotes multiple myeloma progression by adsorbing miR-610 and upregulating AKT3 expression.

Circular RNAs (circRNAs) play an important regulatory role in a variety of malignancies. Nevertheless, the role of circ_0000142 in multiple myeloma (MM) and its regulatory mechanism remains largely unknown. Real-time polymerase chain reaction was employed to detect the expressions of circ_0000142 and miR-610 in MM tissues and cell lines. The expression of AKT3 and apoptosis-related proteins (Bcl-2, Bax) in MM cells was detected by western blot. The correlation between the expression level of circ_0000142 and the clinicopathological parameters of MM patients was analysed. Cell proliferation, apoptosis, migration and invasion were monitored by Cell Counting Kit 8 assay, flow cytometry analysis and Transwell assay, respectively. The dual-luciferase reporter gene assay and RNA immunoprecipitation assay were employed to verify the targeting relationship between circ_0000142 and miR-610. In this study, it was demonstrated that, circ_0000142 was highly expressed in MM patients, and its high expression level was significantly associated with increased International Staging System and Durie-Salmon stage. Overexpression of circ_0000142 enhanced MM cell proliferation, migration, invasion and suppressed cell apoptosis, while knocking down circ_0000142 had the opposite effects. Mechanistically, circ_0000142 functioned as a competitive endogenous RNA, directly targeting miR-610 and positively regulating AKT3 expression. In brief, circ_0000142 enhances the proliferation and metastasis of MM cells by modulating the miR-610/AKT3 axis.

LINC00662 contributes to the progression and the radioresistance of cervical cancer by regulating miR-497-5p and CDC25A.

It is reported that long intergenic non-coding RNA 00662 (LINC00662) plays an oncogenic role in tumours. However, the mechanism of LINC00662 in regulating the progression and radiosensitivity of cervical cancer (CC) is not clear. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to detect LINC00662 and miR-497-5p expressions in CC tissues and cells. The expression of cell division cycle 25 A (CDC25A) in CC cells was examined by Western blot. CC cell proliferation was determined by cell counting kit-8 (CCK-8) and BrdU assays. The survival rate of CC cells was evaluated by colony formation assay under different doses of X-ray irradiation. CC cell migration and invasion were probed by Transwell assay. Besides, the interactions between miR-497-5p and LINC00662, and miR-497-5p and the 3'UTR of CDC25A were verified by dual-luciferase reporter assay, RIP assay, and RNA pull-down experiments. We demonstrated that, LINC00662 expression was remarkably raised in CC tissues and cell lines. LINC00662 overexpression promoted proliferation, migration, invasion and radioresistance of CC cells, and LINC00662 knockdown inhibited the above malignant phenotypes of CC cells. In terms of mechanism, LINC00662 facilitated CC progression and radioresistance by adsorbing miR-497-5p and indirectly up-regulating CDC25A expression. In a word, the LINC00662/miR-497-5p/CDC25A axis boosts proliferation and metastasis of CC cells and enhances the radioresistance of cancer cells. SIGNIFICANCE OF THE STUDY: CC poses a threat to the health of women all over the world. In this study, we demonstrated for the first time that LINC00662 expression was remarkably raised in CC tissues and cells. Cellular experiments confirmed that LINC00662 facilitated cell proliferation, migration, invasion and radiation resistance through the miR-497-5p/CDC25A axis, which might be a promising target for CC treatments.