LncRNA BBOX1-AS1 Aggravates the Development of Ovarian Cancer by Sequestering miR-361-3p to Augment PODXL Expression

Yao, Huiping; Chen, Rui; Yang, Yongxiu; Jiang, Juan

doi:10.1007/s43032-020-00366-5

Cited by 22 publications

(30 citation statements)

References 20 publications

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“…Xu et al uncovered that BBOX1-AS1 expression was elevated in cervical cancer, and BBOX1-AS1 could drive cell malignant phenotypes by up-regulating HOXC6 via miR-361-3p and HuR [17]. Yao et al found that BBOX1-AS1 exerted a tumor-promotive effect in ovarian cancer through sequestering miR-361-3p to enhance PODXL expression [18]. Liu et al disclosed that BBOX1-AS1 acted as a sponge for miR-361-3p to induce SH2B1 expression, thereby accelerating cell proliferation and metastasis in colorectal cancer [19].…”

Section: Discussionmentioning

confidence: 99%

“…Hypoxia-induced lncRNA AC020978 facilitates cell proliferation, migration and glycolytic metabolism in NSCL C through controlling PKM2/HIF-1α axis [15]. BBOX1 anti-sense RNA 1 (BBOX1-AS1) was recently clarified as an oncogenic lncRNA in several human tumors, including gastric cancer [16], cervical cancer [17], ovarian cancer [18] and colorectal cancer [19]. Through mining the microarray data of GEO database including GSE18842 and GSE19188, BBOX1-AS1 expression was found to be higher in NSCLC tumor tissues than that in adjacent non-cancerous tissues.…”

Section: Introductionmentioning

confidence: 99%

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KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

Shi

Yang

et al. 2021

J Exp Clin Cancer Res

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Background Non-small cell lung cancer (NSCLC) is a major histological subtype of lung cancer with high mortality and morbidity. A substantial amount of evidence demonstrates long non-coding RNAs (lncRNA) as critical regulators in tumorigeneis and malignant progression of human cancers. The oncogenic role of BBOX1 anti-sense RNA 1 (BBOX1-AS1) has been reported in several tumors. As yet, the potential functions and mechanisms of BBOX1-AS1 in NSCLC are obscure. Methods The gene and protein expression was detected by qRT-PCR and western blot. Cell function was determined by CCK-8, colony forming, would healing and transwell assays. Bioinformatics tools, ChIP assays, dual luciferase reporters system and RNA pull-down experiments were used to examine the interaction between molecules. Subcutaneous tumor models in nude mice were established to investigate in vivo NSCLC cell behavior. Results BBOX1-AS1 was highly expressed in NSCLC tissues and cells. High BBOX1-AS1 expression was associated with worse clinical parameters and poor prognosis. BBOX1-AS1 up-regulation was induced by transcription factor KLF5. BBOX1-AS1 deficiency resulted in an inhibition of cell proliferation, migration, invasion and EMT in vitro. Also, knockdown of BBOX1-AS1 suppressed NSCLC xenograft tumor growth in mice in vivo. Mechanistically, BBOX1-AS1 acted act as a competetive “sponge” of miR-27a-5p to promote maternal embryonic leucine zipper kinase (MELK) expression and activate FAK signaling. miR-27a-5p was confirmed as a tumor suppressor in NSCLC. Moreover, BBOX1-AS1-induced increase of cell proliferation, migration, invasion and EMT was greatly reversed due to the overexpression of miR-27a-5p. In addition, the suppressive effect of NSCLC progression owing to BBOX1-AS1 depletion was abated by the up-regulation of MELK. Consistently, BBOX1-AS1-mediated carcinogenicity was attenuated in NSCLC after treatment with a specific MELK inhibitor OTSSP167. Conclusions KLF5-induced BBOX1-AS1 exerts tumor-promotive roles in NSCLC via sponging miR-27a-5p to activate MELK/FAK signaling, providing the possibility of employing BBOX1-AS1 as a therapeutic target for NSCLC patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

Shi

Yang

et al. 2021

J Exp Clin Cancer Res

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“…lncRNAs, which can serve as critical tumor promoters or suppressors, can affect the occurrence and progression of multiple types of diseases (23,24). HAGLROS is abnormally expressed in the serum of patients with pneumonia and it has been found to decrease apoptosis and autophagy in lipopolysaccharide-induced WI-38 cells (25).…”

Section: Discussionmentioning

confidence: 99%

Interference of long non‑coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR‑26b‑5p

Zhu¹,

Mei

2021

Exp Ther Med

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Ovarian cancer (OV) is the fifth most common type of cancer affecting women worldwide. Long non-coding RNAs (lncRNAs) serve essential roles in the progression of OV. As such, the present study aimed to investigate the specific role of HAGLR opposite strand lncRNA (HAGLROS) in OV and the underlying mechanism of action through which HAGLROS exerts its effects on OV cells. In the present study, the expression of HAGLROS in several OV cell lines was first detected using reverse transcription-quantitative PCR. HAGLROS was then silenced to evaluate cell viability, proliferation and apoptosis, which were determined using Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Additionally, immunofluorescence staining and western blotting were used to confirm the expression profile of proliferation-and apoptosis-related proteins. Moreover, a dual luciferase reporter assay was used to verify the potential interactions between HAGLROS and microRNA (miR)-26b-5p. Subsequently, rescue assays were performed to investigate the effects of HAGLROS and miR-26b-5p on OV progression. The results indicated that HAGLROS was highly expressed in OV cells. Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. miR-26b-5p inhibitor transfection partially reversed the effects of HAGLROS knockdown on the proliferation and apoptosis of OV cells. In conclusion, the results of the present study suggested that interference of HAGLROS suppressed the proliferation and promoted the apoptosis of OV cells through regulating miR-26b-5p, indicating that HAGLROS may be a promising biomarker in OV diagnosis and treatment.

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“…The dual role of miR‐361‐3p in human carcinogenesis as either tumor inhibitors or tumor drivers has been highlighted (for instance): miR‐361‐3p contributes to the development of pancreatic cancer 31 and breast cancer 32 ; miR‐361‐3p works as a strong anticancer factor in lymphoma 33 and ovarian cancer. 34 The contradictory findings may be attributed to the different types of tumors in these reports. In line with previous studies showing the anticancer activity of miR‐361‐3p in NSCLC, 14 , 15 , 16 we uncovered that miR‐361‐3p hinders the growth and metastasis of H1299/DDP and A549/DDP cells and sensitizes them to DDP therapy.…”

Section: Discussionmentioning

confidence: 90%

“…Here, we first ascertained that circ_0058357 harbors a miR‐361‐3p binding site, and the effects of circ_0058357 inhibition are partially due to the elevation of miR‐361‐3p. The dual role of miR‐361‐3p in human carcinogenesis as either tumor inhibitors or tumor drivers has been highlighted (for instance): miR‐361‐3p contributes to the development of pancreatic cancer 31 and breast cancer 32 ; miR‐361‐3p works as a strong anticancer factor in lymphoma 33 and ovarian cancer 34 . The contradictory findings may be attributed to the different types of tumors in these reports.…”

Section: Discussionmentioning

confidence: 99%

Identification of circ_0058357 as a regulator in non‐small cell lung cancer cells resistant to cisplatin by miR‐361‐3p/ABCC1 axis

Chu

et al. 2021

Thoracic Cancer

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Background Drug resistance is a major clinical drawback behind the failure of chemotherapy in non‐small cell lung cancer (NSCLC). In this study, we undertook to identify the precise role of circular RNA (circRNA) circ_0058357 in the functional properties of DDP‐resistant NSCLC cells. Methods Circ_0058357, miR‐361‐3p and ATP‐binding cassette (ABC) subfamily C member 1 (ABCC1) were quantified by qRT‐PCR and western blot. Cell survival and viability were gauged by MTT assay. Cell proliferation, apoptosis, invasion and migration were measured by EdU, flow cytometry, transwell and wound‐healing assays, respectively. The direct relationship between miR‐361‐3p and circ_0058357 or ABCC1 was validated by dual‐luciferase reporter assay. Results Our data showed that circ_0058357 was highly expressed in DDP‐resistant NSCLC tissues and cells. Inhibition of circ_0058357 repressed cell growth, invasion, migration, and promoted DDP sensitivity and cell apoptosis of H1299/DDP and A549/DDP cells in vitro. Moreover, inhibition of circ_0058357 diminished the growth of A549/DDP cells and sensitized them to the cytotoxic effect of DDP in vivo. Mechanistically, circ_0058357 contained a miR‐361‐3p binding site and miR‐361‐3p was identified as a molecular mediator of circ_0058357 regulation. MiR‐361‐3p suppressed ABCC1 expression by binding to ABCC1 3′UTR, and miR‐361‐3p‐mediated inhibition of ABCC1 affected the growth, invasion, migration, apoptosis and DDP sensitivity of H1299/DDP and A549/DDP cells. Furthermore, circ_0058357 regulated ABCC1 expression by competitively binding to shared miR‐361‐3p. Conclusions Our findings identified that inhibition of circ_0058357 suppresses the growth and metastasis of H1299/DDP and A549/DDP cells and sensitizes them to DDP therapy partially by targeting the miR‐361‐3p/ABCC1 axis.

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LncRNA BBOX1-AS1 Aggravates the Development of Ovarian Cancer by Sequestering miR-361-3p to Augment PODXL Expression

Cited by 22 publications

References 20 publications

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

Interference of long non‑coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR‑26b‑5p

Identification of circ_0058357 as a regulator in non‐small cell lung cancer cells resistant to cisplatin by miR‐361‐3p/ABCC1 axis

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