Long non-coding RNA ARAP1-AS1 accelerates cell proliferation and migration in breast cancer through miR-2110/HDAC2/PLIN1 axis

Abstract

Breast cancer (BC) poses a great threaten to women health. Numerous evidences suggest the important role of long non-coding RNAs (lncRNAs) in BC development. In the present study, we intended to investigate the role of ARAP1-AS1 in BC progression. First of all, the GEPIA data suggested that ARAP1-AS1 was highly expressed in breast invasive carcinoma (BRAC) tissues compared with the normal breast tissues. Meanwhile, the expression of ARAP1-AS1 was greatly up-regulated in BC cell lines. ARAP1-AS1 knockdown led to repressed proliferation, strengthened apoptosis and blocked migration of BC cells. Moreover, ARAP1-AS1 could boost HDAC2 expression in BC through sponging miR-2110 via a ceRNA mechanism. Of note, the UCSC predicted that HDAC2 was a potential transcriptional regulator of PLIN1, an identified tumor suppressor in BC progression. Moreover, we explained that the repression of HDAC2 on PLIN1 was owing to its deacetylation on PLIN1 promoter. More importantly, depletion of PLIN1 attenuated the mitigation function of ARAP1-AS1 silence on the malignant phenotypes of BC cells. To sum up, ARAP1-AS1 serves a tumor-promoter in BC development through modulating miR-2110/HDAC2/PLIN1 axis, which may help to develop novel effective targets for BC treatment.

Low expression of long non-coding RNA ARAP1-AS1 can inhibit lung cancer proliferation by inducing G0/G1 cell cycle organization

“…Moreover, lncRNA ARAP1-AS1 is also highly expressed in breast invasive carcinoma tissues, and the expression of lncRNA ARAP1-AS1 is significantly upregulated in breast cancer cell lines. The down-regulation of lncRNA ARAP1-AS1 expression leads to inhibition of breast cancer cell proliferation, enhanced apoptosis, and blocked migration (19). In the present study, it was found that lncRNA ARAP1-AS1 was significantly up-regulated in lung cancer tissues and cells, and knocking down of lncRNA ARAP1-AS1 can significantly inhibit cell proliferation and clonal formation.…”

“…Furthermore, studies have shown that the non-coding RNA, ARAP1 antisense RNA 1 (ARAP1-AS1), can markedly affect the occurrence and development of other tumors, including bladder, colorectal, and breast cancers (17)(18)(19). However, the expression level, biological function, and molecular function of lncRNA ARAP1-AS1 in lung cancer tissues are still unclear.…”

“…After the cells were cultured overnight, the fusion reached 80%. SuperFectin short hairpin RNA (shRNA) transfection reagent was used to combine shARAP1-AS1 (shRNA-1 and shRNA-2) with negative control shRNA (shNC) transfection cells, and the primer sequence was interfered with reference (19). After 48 hours, quantitative RT-PCR (qRT-PCR) and Western blotting were performed to detect transfection efficiency.…”

Characterization of the Relationship Between the Expression of Aspartate β-Hydroxylase and the Pathological Characteristics of Breast Cancer

“…High levels of LEP expression were associated with good prognosis in our study, which differed from an earlier report indicating LEP overexpression in BC [ 31 ]. PLIN1 promotes BC cell proliferation and migration [ 32 ]. CAV1 plays a key role in the stress response of BC cells by regulating lysosomal function and autophagy [ 33 ].…”

Construction of an mRNA-miRNA-lncRNA network prognostic for triple-negative breast cancer

“…Zhao et al suggested that the lncRNA TUSC8 may affect epithelial-mesenchymal transition (EMT)-associated protein levels by functioning as a ceRNA of myosin regulatory light chain interacting protein (MYLIP) as it binds miR-190b-5p, leading to the suppression of breast cancer progression [ 19 ]. Lu et al found that lncARAP1-AS promotes tumorigenesis by enhancing the proliferative and migratory abilities of breast cancer cells by modulating the miR-2110/HDAC2/PLIN1 axis [ 20 ]. However, there are different breast cancer subtypes, including HER2-positive breast cancer, luminal A and B breast cancer, and TNBC, and comprehensive studies on the ceRNA networks in each breast cancer subtype are limited, particularly regarding the identification of their specific molecular mechanisms.…”