LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis

Abstract

Background Lung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD. Methods The expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student’s t test or one-way analysis of variance. Results LINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells. Conclusion LINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.

Preparation, characterisation, and in vitro cancer‐suppression function of RNA nanoparticles carrying miR‐301b‐3p Inhibitor

“…[ 41 ].Western blot assay implied that γH2AX and Bax protein levels were upregulated and Bcl‐2 expression was downregulated in response to NPs and DDP treatment, indicating that miR‐301b‐3p Inhibitor in materials was able to enhance DDP sensitivity and induce cell apoptosis. This correlates with previous findings that miR‐301b‐3p is involved in apoptosis in cancers [ 42 , 43 , 44 ]. MiR‐301b‐3p Inhibitor and A549apt synergised more prominently than those NPs without A549apts.…”

“…With the help of A549apts, miR-301b-3p Inhibitor could better target cancer cells, which provides evidence in support of the finding that downregulation of miR-301b-3p increases the sensitivity of cancer cells to cisplatin as proposed by Zhu et al [41].Western blot assay implied that γH2AX and Bax protein levels were upregulated and Bcl-2 expression was downregulated in response to NPs and DDP treatment, indicating that miR-301b-3p Inhibitor in materials was able to enhance DDP sensitivity and induce cell apoptosis. This correlates with previous findings that miR-301b-3p is involved in apoptosis in cancers [42][43][44]. MiR-301b-3p Inhibitor and A549apt synergised more prominently than those NPs without A549apts.…”

Differential expression and clinical significance of long non-coding RNAs in the development and progression of lung adenocarcinoma

“…Qian et al. ( 48 ) found that LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis. Xiong et al.…”

“…Wang et al (47) found that LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression. Qian et al (48) found that LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis. Xiong et al (49) found that LncRNA NEAT1 may compete with USF1 for binding to miR-193a-3p as a ceRNA and accelerates lung adenocarcinoma deterioration.…”

LNC01089-LINC00963/miR-1244-5p/IGF1 ceRNA axis might regulate FOXO signaling pathway in breast cancer patients: a biomarker discovery investigation

“…In addition to breast cancer, LNC01089 contributed to the development of other cancer types. For example, based on the study of Qian et al in 2021, in lung cancer cells, LNC01089 regulates the miR-301b-3p/STARD13 interaction axis, and through this mechanism, this lncRNA could decrease the migration rate of BC cells(Qian et al, 2021). LNC01089 also regulates the miR-27b-3p/FBLN5 axis in thyroid cancer patients, and this mechanism could suppress the malignant development(Pan et al, 2022)There has been no previous research on the diagnostic utility of LNC01089 across any cancer form, and for the rst time, we showed that this lncRNA has a signi cant diagnostic capability for distinguishing cancer samples from normal samples based on ROC analysis.…”