LINC00319 Promotes Cervical Cancer Progression Via Targeting miR-147a/IGF1R Pathway

Ma, Zhe; Cai, Yufei; Zhang, Limei; Tian, Chenchen; Lyu, Lin

doi:10.1089/cbr.2020.3722

Cited by 14 publications

(15 citation statements)

References 33 publications

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“…Bioinformatics software analysis showed that miR-147a could be targeted by lncRNA HOTAIR. In cancer-related studies, miR-147a has been identified as a tumor suppressor to regulate cancer progression, such as non-small-cell lung cancer [ 24 ] and cervical cancer [ 25 ]. MiR-147a might inhibit cellular inflammation to mitigate pneumonia process [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

Wang

Huangfu

et al. 2022

Diabetol Metab Syndr

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Background Long non-coding RNAs (lncRNAs) have been shown to be involved in the regulation of many disease progression. However, the role of lncRNA HOX transcript antisense RNA (HOTAIR) in diabetic nephropathy (DN) remains unclear. Methods High glucose (HG)-induced human mesangial cells (HMC) was used to construct DN cell models in vitro. HMC proliferation was evaluated by CCK8 assay and EDU staining. Protein levels of proliferation markers, fibrosis markers, and wingless-type family member 2B (WNT2B) were measured using western blot analysis. HMC oxidative stress was assessed by determining the levels of oxygen species and malondialdehyde, as well as superoxide dismutase activity. Relative expression levels of lncRNA HOTAIR, microRNA (miR)-147a, and WNT2B were examined using quantitative real-time PCR. The interaction between miR-147a and lncRNA HOTAIR or WNT2B was confirmed by dual-luciferase reporter assay and RIP assay. Results Our data showed that lncRNA HOTAIR knockdown could inhibit the proliferation, fibrosis, and oxidative stress in HG-induced HMC. LncRNA HOTAIR could serve as a sponge of miR-147a. The inhibition effect of lncRNA HOTAIR silencing on the biological functions of HG-induced HMC could be reversed by miR-147a inhibitor. WNT2B was targeted by miR-147a, and its overexpression also overturned the suppressive effect of miR-147a on the proliferation, fibrosis, and oxidative stress of HG-induced HMC. Conclusion In total, our research pointed out that lncRNA HOTAIR could mediate miR-147a/WNT2B axis to promote DN progression.

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Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

Wang

Huangfu

et al. 2022

Diabetol Metab Syndr

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“…Linc00319 silencing has suppressed cell proliferation, invasion, and migration of cervical cancer cells. This lncRNA interacts with miR-147a to modulate the expression of IGF1R ( Ma et al, 2020 ). DBH-AS1 is another oncogenic lncRNA in hepatocellular carcinoma.…”

Section: Igf-associated Lncrnas In Human Disordersmentioning

confidence: 99%

“…Additionally, downregulation of circVANGL1 through suppressing the expression level of IGFBP2 could attenuate breast cancer cell invasion, migration, and proliferation ( Yang D. et al, 2020 ). Also, IRAIN, Linc00319, and DLEU1 through negatively regulating IGF-1R could cause breast cancer, cervical cancer, and hepatocellular carcinoma ( Pian et al, 2018 ; Zhang W. et al, 2019 ; Ma et al, 2020 ). Figure 3 summarizes the role of these IGF-associated lncRNAs in human disorders.…”

Section: Igf-associated Lncrnas In Human Disordersmentioning

confidence: 99%

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

Ghafouri‐Fard

Abak

Mohaqiq

et al. 2021

Front. Cell Dev. Biol.

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The insulin-like growth factors (IGFs) are polypeptides with similar sequences with insulin. These factors regulate cell growth, development, maturation, and aging via different processes including the interplay with MAPK, Akt, and PI3K. IGF signaling participates in the pathogenesis of neoplasia, insulin resistance, diabetes mellitus, polycystic ovarian syndrome, cerebral ischemic injury, fatty liver disease, and several other conditions. Recent investigations have demonstrated the interplay between non-coding RNAs and IGF signaling. This interplay has fundamental roles in the development of the mentioned disorders. We designed the current study to search the available data about the role of IGF-associated non-coding RNAs in the evolution of neoplasia and other conditions. As novel therapeutic strategies have been designed for modification of IGF signaling, identification of the impact of non-coding RNAs in this pathway is necessary for the prediction of response to these modalities.

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“…In this paper, IFG1R might be a strong candidate as a downstream effector of miR-296-5p function because of its oncogenic property in various cancers, including cervical cancer and small intestinal carcinoma. 23 , 24 Our data first showed that miR-296-5p directly targeted IFG1R, and IGF1R was an important mediator of circ_0067835 function in CRC cells. However, the direct evidence between the miR-296-5p/IFG1R axis and circ_0067835-mediated CRC development and radiosensitivity in vivo was absent, which was expected to be investigated in further work.…”

Section: Discussionmentioning

confidence: 81%

Circ_0067835 Knockdown Enhances the Radiosensitivity of Colorectal Cancer by miR-296-5p/IGF1R Axis

Wang¹,

Sun²,

Yang³

et al. 2021

OTT

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Background: Colorectal cancer (CRC) is one of the most common malignant cancers globally. Circular RNAs (circRNAs) have been implicated in the development of CRC. In this paper, we set to explore the precise action of circ_0067835 in CRC progression and radioresistance. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of circ_0067835, microRNA-296-5p (miR-296-5p) and insulin-like growth factor 1 receptor (IGF1R). Western blot was used to measure the level of IGF1R protein. Cell proliferation, cell cycle distribution and apoptosis were determined by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry and caspase-3 activity assays, respectively. The direct relationship between miR-296-5p and circ_0067835 or IGF1R was verified by dual-luciferase reporter assays. Additionally, in vivo assays were applied to confirm the role of circ_0067835 in vivo. Results: Exosomal circ_0067835 was upregulated in the serum of CRC patients after radiotherapy. Exosome-mediated circ_0067835 knockdown repressed cell proliferation, cell cycle progression, and enhanced cell apoptosis and radiosensitivity in vitro. Circ_0067835 sponged miR-296-5p to regulate IGF1R expression in CRC cells. Moreover, the knockdown of circ_0067835 regulated CRC cell behaviors by up-regulating miR-296-5p and downregulating IGF1R in vitro. Furthermore, circ_0067835 knockdown diminished tumor growth and promoted cell radiosensitivity in vivo. Conclusion: Circ_0067835 knockdown suppressed CRC progression and enhanced CRC cell radiosensitivity partially by the miR-296-5p/IGF1R axis. The findings established a rationale that targeting circ_0067835 might be a promising point for improving CRC treatment.

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LINC00319 Promotes Cervical Cancer Progression Via Targeting miR-147a/IGF1R Pathway

Cited by 14 publications

References 33 publications

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia

Circ_0067835 Knockdown Enhances the Radiosensitivity of Colorectal Cancer by miR-296-5p/IGF1R Axis

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