Long noncoding RNA CCDC183-AS1 depletion represses breast cancer cell proliferation, colony formation, and motility by sponging microRNA-3918

Many studies have illustrated the significance of long noncoding RNAs in oncogenesis and promotion of breast cancer(BC).However,the biological roles of CCDC183 antisense RNA 1(CCDC183-AS1)in BC have rarely been characterized.Thus,we explored whether CCDC183-AS1 is involved in the malignancy of BC and elucidated the possible underlying mechanisms.Our data confirmed elevated CCDC183-AS1 expression in BC,which was associated with poor clinical outcomes.Functionally,knocking down CCDC183-AS1 hampered cell proliferation,colony formation,migration,and invasion in BC.Additionally,the absence of CCDC183-AS1 restrained tumor growth in vivo.Mechanistically,CCDC183-AS1 executed as a competitive endogenous RNA in BC cells by decoying microRNA-3918(miR-3918)and consequently overexpressing fibroblast growth factor receptor 1(FGFR1).Furthermore,functional rescue experiments confirmed that inactivation of the miR-3918/FGFR1 regulatory axis by inhibiting miR-3918 or increasing FGFR1 expression could abrogate the CCDC183-AS1 ablation-mediated repressive effects in BC cells.In summary,CCDC183-AS1 deteriorates the malignancy of BC cells by controlling miR-3918/FGFR1 regulatory axis.We believe that our study can deepen our understanding of BC etiology and contribute to an improvement in treatment choices.

Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

Long noncoding RNA PPP1R14B antisense RNA 1(PPP1R14B-AS1)has emerged as a critical modulator of liver cancer and lung adenocarcinoma progression.However,the functional importance and biological relevance of PPP1R14B-AS1 in breast cancer remain unclear.Therefore,this study was designed to detect PPP1R14B-AS1 levels in breast cancer cells using qRT–PCR and elucidate the influence of PPP1R14B-AS1 on aggressive phenotypes.Furthermore,molecular events mediating the action of PPP1R14B-AS1 were characterized in detail.Functional experiments addressed the impacts of PPP1R14B-AS1 knockdown on breast cancer cells.In this study,PPP1R14B-AS1 was found to be overexpressed in breast cancer,exhibiting a close correlation with poor patient prognosis.Results also showed that breast cancer cell proliferation and motility were suppressed when PPP1R14B-AS1 was silenced.Mechanistically,PPP1R14B-AS1 acted as a competing endogenous RNA for microRNA-134-3p(miR-134-3p)in breast cancer cells.PPP1R14B-AS1 also increased LIM and SH3 protein 1(LASP1)levels by imitating miR-134-3p in breast cancer cells.Rescue experiments further corroborated that the knockdown of miR-134-3p or an increase in LASP1 restored the aggressive malignant characteristics of breast cancer cells that were weakened by PPP1R14B-AS1 depletion.In summary,PPP1R14B-AS1 facilitated the oncogenicity of breast cancer cells by controlling the miR-134-3p/LASP1 axis.We believe that ourfindings may contribute to the development of precision therapy techniques in thefield of breast cancer treatment.

Long noncoding RNA LINC02568 sequesters microRNA-874-3p to facilitate malignancy in breast cancer cells via cyclin E1 overexpression

Increasing numbers of long noncoding RNAs(lncRNAs)are implicated in breast cancer oncogenicity.However,the contribution of LINC02568 toward breast cancer progression remains unclear and requires further investigation.Herein,we evaluated LINC02568 expression in breast cancer and clarified its effect on disease malignancy.We also investigated the mechanisms underlying the pro-oncogenic role of LINC02568.Consequently,LINC02568 was upregulated in breast cancer samples,with a notable association with worse overall survival.Functionally,depleted LINC02568 suppressed cell proliferation,colony formation,and metastasis,whereas LINC02568 overexpression exerted the opposite effects.Our mechanistic investigations suggested that LINC02568 was physically bound to and sequestered microRNA-874-3p(miR-874-3p).Furthermore,miR-874-3p mediated suppressive effects in breast cancer cells by targeting cyclin E1(CCNE1).LINC02568 positively controlled CCNE1 expression by sequestering miR-874-3p.Rescue experiments revealed that increased miR-874-3p or decreased CCNE1 expression recovered cell growth and motility functions induced by LINC02568 in breast cancer cells.In conclusion,the tumor-promoting functions of LINC02568 in breast cancer cells were enhanced by sequestering miR-874-3p and consequently over-expressing CCNE1.Our data may facilitate the identification of novel therapeutic targets in clinical settings.