LIFR-AS1 modulates Sufu to inhibit cell proliferation and migration by miR-197-3p in breast cancer

Xu, Fangfang; Hu, Chengjiu

doi:10.1042/bsr20180551

Cited by 34 publications

(29 citation statements)

References 38 publications

(37 reference statements)

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“…As expected, the interaction between miR-197-3p and TUSc8 was confirmed by luciferase reporter and RIP assays. According to previous studies, miR-197-3p plays an oncogenic role in breast cancer, bladder cancer and thyroid cancer (19,20,42,43). However, the anti-oncogenic role of miR-197-3p has been found in prostate cancer and gastric cancer (44,45).…”

Section: Discussionmentioning

confidence: 98%

“…3B). It has been reported that miR-197-3p serves as a tumour promoter in various types of cancer (19,27); thus, miR-197-3p was analysed in subsequent explorations. It was observed that miR-197-3p expression was substantially increased by transfection with miR-197-3p mimic in the MG-63 and U2OS cells (Fig.…”

Section: Tusc8 Is Prominently Downregulated In Os Tissues and Cellsmentioning

confidence: 99%

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TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

et al. 2020

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Osteosarcoma (OS) is one of the most common malignant bone tumours and generally occurs in children and adolescents. Increasing evidence has demonstrated that dysregulated long non-coding RNAs (lncRNAs) play crucial roles in the progression of various human neoplasms. Among these, tumour suppressor candidate 8 (TUSc8) is a novel lncRNA and has been reported to function as a tumour suppressor in cervical cancer. However, the exact role of TUSc8 in OS remains largely unknown. In the present study, it was observed that TUSc8 was markedly downregulated in OS tissues and cell lines. Functional experiments demonstrated that the overexpression of TUSC8 significantly suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), whereas it accelerated the apoptosis of OS cells. Mechanistically, TUSc8 served as a sponge for miR-197-3p, and EH-domain containing 2 (EHd2) was identified as a downstream target molecule of miR-197-3p. Further investigations indicated that EHD2 knockdown significantly reversed the effects on OS cellular processes induced by TUSC8 overexpression. On the whole, these findings indicate that TUSc8 functions as a competing endogenous RNA (ceRNA) to suppress OS cell growth and EMT via the miR-197-3p/EHd2 axis. TUSc8 may thus function as a potential therapeutic target in OS treatment.

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Section: Discussionmentioning

confidence: 98%

Section: Tusc8 Is Prominently Downregulated In Os Tissues and Cellsmentioning

confidence: 99%

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

et al. 2020

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“…miR-197-3p, as an oncogenic miRNA, has been reported to promote cell proliferation, migration, and invasion in bladder cancer cells [12]. Moreover, LIFR-AS1 inhibits breast cancer cell proliferation and migration by binding to miR-197-3p [13]. In lung cancer cells, the miR-197-3p/p120 catenin axis is regulated by lncRNA MALAT1 to depress chemo-sensitivity [14].…”

Section: Ivyspringmentioning

confidence: 99%

miR-197-3p Represses the Proliferation of Prostate Cancer by Regulating the VDAC1/AKT/β-catenin Signaling Axis

Huang

et al. 2020

Int. J. Biol. Sci.

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Accumulating investigations have demonstrated that microRNAs (miRNAs) are promising efficient targets for the next generation of molecular therapeutics. The development of miRNA-based therapies requires the identification and validation of cancer-associated miRNAs. Herein, we identified that miR-197-3p regulates the carcinogenesis and development of prostate cancer (PCa) via bioinformatics analysis. Next, we investigated the function and regulatory mechanisms of miR-197-3p in PCa. Overexpression of miR-197-3p suppressed PCa cell proliferation and colony formation. In contrast, inhibition of miR-197-3p activity enhanced PCa cell proliferation and colony formation. Mechanistic investigations identified that voltage dependent anion channel 1 (VDAC1) is a direct target of miR-197-3p. miR-197-3p targeting of VDAC1 resulted in downregulation of p-Akt and β-catenin. Subsequently, we found that restoration of VDAC1 abolished the effects of miR-197-3p on PCa cell proliferation and AKT signaling pathway. Furthermore, we confirmed that miR-197-3p suppressed tumor xenograft growth in vivo. In conclusion, our study offers an empirical investigation of miR-197-3p, a tumor suppressor that may be a potential therapeutic target in PCa.

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“…A previous study reported that LIFR-AS1 inhibits the proliferation and survival of colorectal cancer cells [10]. Another study demonstrated that LIFR-AS1 has the ability to control breast cancer cell proliferation and migration [11]. However, the role of LIFR-AS1 in NSCLC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…miRNAs are small, endogenous non-coding RNAs that are capable of repressing gene expression by binding to the 3′-untranslated region (3′-UTR) of target mRNAs [10]. Compelling evidence indicates that lncRNAs can work as competitive endogenous RNA (ceRNA) for miRNAs [9,11,12]. For example, the lncRNA MALAT1 antagonizes the activity of miR-199a to promote ZHX1 expression, leading to increased glioblastoma cell proliferation and survival [12].…”

Section: Introductionmentioning

confidence: 99%

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

Wang

Huang

et al. 2020

Cancer Cell Int

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Background: MicroRNA 942-5p (miR-942-5p) has been reported to promote migration and invasion in non-small cell lung cancer (NSCLC), but the underlying mechanism is not completely understood. The interplay between long noncoding RNAs (lncRNAs) and miRNAs plays a crucial role in tumor progression. Methods: In the present study, we performed bioinformatic and biochemical analyses to identify miR-942-5p-interacting lncRNAs. The function and clinical significance of the candidate lncRNA(s) in NSCLC were determined. Results: We identified LIFR-AS1 as a pivotal miR-942-5p-interacting lncRNA. Overexpression of miR-942-5p caused a reduction of LIFR-AS1 in NSCLC cells. LIFR-AS1 showed the ability to sponge miR-942-5p, leading to derepression of ZNF471. Functionally, LIFR-AS1 overexpression inhibited NSCLC cell migration and invasion, whereas LIFR-AS1 silencing yielded an opposite effect. In vivo studies confirmed that LIFR-AS1 overexpression suppressed lung metastasis of NSCLC cells. Rescue experiments demonstrated that enforced expression of miR-942-5p or depletion of ZNF471 restored the migration and invasion capacity of LIFR-AS1-overexpressing cells. Moreover, overexpression of ZNF471 restrained NSCLC cell invasion. Clinically, LIFR-AS1 downregulation was significantly correlated with TNM stage, lymph node metastasis, and reduced overall survival in NSCLC patients. Conclusions: we provide first evidence for the involvement of the LIFR-AS1/miR-942-5p/ZNF471 axis in NSCLC invasion and metastasis. LIFR-AS1 may represent a novel target for the treatment of NSCLC.

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LIFR-AS1 modulates Sufu to inhibit cell proliferation and migration by miR-197-3p in breast cancer

Cited by 34 publications

References 38 publications

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

TUSC8 inhibits the development of osteosarcoma by sponging miR‑197‑3p and targeting EHD2

miR-197-3p Represses the Proliferation of Prostate Cancer by Regulating the VDAC1/AKT/β-catenin Signaling Axis

lncRNA LIFR-AS1 suppresses invasion and metastasis of non-small cell lung cancer via the miR-942-5p/ZNF471 axis

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