Effects of LncRNA Lnc-LIF-AS on cell proliferation, migration and invasion in a human cervical cancer cell line

Song, Weiguo; Wang, Juan; Liu, Hanyuan; Zhu, Chenchen; Xu, Fei; Qian, Lili; Shen, Zhen; Zhu, Jing; Yin, Shuai; Qin, Jiwei; Chen, Liang; Wu, Dexiang; Nashan, Björn; Ge, Shengfang; Xiao, Weihua; Ying, Zhe

doi:10.1016/j.cyto.2019.05.004

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…As molecular regulators that have attracted increasing attention in recent years, long non-coding RNAs (lncRNAs) can control basic biological processes and tumor progression, and research on them is conducive to better understanding the gene regulatory network of cancer [7,8]. The lncRNA family not only plays a role in the development of gynecological tumors such as breast cancer, cervical cancer and endometrial cancer, but participates in the pathological mechanism of OC [9][10][11][12]. For example, CACS15 can promote the malignant development of OC by recruiting EZH2 to suppress the expression of APC, and DANCR can mediate tumor growth and angiogenesis of OC by targeting regulation of microRNA (miR)-145 [13,14].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer

Dai

Guo

et al. 2020

Bioscience Reports

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Purpose: To investigate the regulation mechanism of long non-coding RNA (lncRNA) plasmocytoma variant translocation 1 (PVT1) in ovarian cancer (OC). Methods: The levels of PVT1, microRNA (miR)-543, serpin peptidase inhibitor-clade I (neuroserpin)-member 1 (SERPINI1) in OC tissues and OVCAR-3, A2780, TOV-112D of OC cell lines were detected by quantitative real-time PCR (qRT-PCR) and Western Blot (WB). Cell proliferation, migration, invasion, apoptosis and the regulatory relationship between genes and target genes were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell, flow cytometry and dual luciferase reporter (DLR). The OC patients were followed up for 5 years to analyze the relationship between PVT1 and 5-year overall survival (OS). Results: In contrast with miR-543, PVT1 and SERPINI1 were highly expressed in OC tissues and cell lines, and high levels of PVT1 were significantly associated with lower 5-year OS of patients. Down-regulating PVT1 not only inhibited the malignant proliferation, migration and invasion of OC cells, but promoted cell apoptosis. PVT1 regulated miR-543 in a targeted manner, and its overexpression could attenuate the anticancer effect of miR-543 on OC cells. In addition, miR-543 also directly targeted SERPINI1, and miR-543 knockdown weakened the inhibitory effect of down-regulated SERPINI1 on OC progression. Furthermore, we found that PVT1 acted as a competitive endogenous RNA to sponge miR-543, thereby regulating the expression of SERPINI1. Conclusion: PVT1 can mediate the molecular mechanism of OC by miR-543/SERPINI1 axis regulatory network, which is a new therapeutic direction for OC.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer

Dai

Guo

et al. 2020

Bioscience Reports

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“…They are transcripts longer than 200 nucleotides that are not translated into proteins. They act as important regulators in many human cancers, such as prostate cancer, bladder cancer and cervical cancer . Small nucleolar RNA host gene 1 (SNHG1) located at the region of chromosome 11 has been identified to be associated with the occurrence of multiple human cancers, including NSCLC .…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non‐small cell lung cancer cells via the miR‐361‐3p/FRAT1 axis

Zheng

2019

Thoracic Cancer

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Background: Non-small-cell lung cancer (NSCLC) is the most lethal type of cancer. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as crucial regulators in the development of NSCLC. The aim of our study was to explore the molecular mechanism of SNHG1 to enable better treatment for NSCLC patients. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of Small nucleolar RNA host gene 1 (SNHG1), miR-361-3p and frequently rearranged in advanced T-cell lymphomas 1 (FRAT1). The protein level of FRAT1 was measured by western blot assay. Cell proliferation was evaluated by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells were counted by transwell assay. The relationship between miR-361-3p and SNHG1 or FRAT1 was confirmed by dual-luciferase reporter assay. Results: Our results indicated that SNHG1 and FRAT1 were highly expressed in NSCLC tissues and cells. SNHG1 silencing inhibited proliferation, induced apoptosis and blocked migration and invasion of NSCLC cells. Also, FRAT1 downregulation suppressed proliferation, promoted apoptosis and hindered migration and invasion of NSCLC cells. Further, FRAT1 could recover the effects of SNHG1 silencing on proliferation, apoptosis, migration and invasion of NSCLC cells. SNHG1 sponged miR-361-3p and negatively regulated miR-361-3p expression. Meanwhile, miR-361-3p targeted FRAT1 and inversely modulated FRAT1 expression. In addition, miR-361-3p inhibition abated the effect of SNHG1 knockdown on FRAT1 expression. Conclusion: In conclusion, LncRNA SNHG1 promoted the proliferation, repressed apoptosis and enhanced migration and invasion of NSCLC cells by regulating FRAT1 expression via sponging miR-361-3p.

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“…Western blot was performed as previously described. 23 First, Ishikawa cells were collected and mixed with RIPA lysis buffer, and the cell supernatant lysed by RIPA lysis buffer (Abcam, Cambridge, UK) was obtained by centrifugation. The protein concentration was determined using a protein BCA kit (Abcam) to ensure that the concentrations were consistent between the control and the experimental groups.…”

Section: Methodsmentioning

confidence: 99%

Growth hormone inhibits the JAK/STAT3 pathway by regulating SOCS1 in endometrial cells <em>in vitro</em>: a clue to enhance endometrial receptivity in recurrent implantation failure

Sun

Zhu

et al. 2022

Eur J Histochem

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Recurrent implantation failure (RIF) is defined as failure to achieve clinical pregnancy after at least 3 transfers of good-quality embryos by natural or artificial means. RIF is often a complex problem with a wide variety of etiologies and mechanisms as well as treatment options. In this study, using immunohistochemistry and Western blot, we demonstrated that the expression of leukemia inhibitory factor (LIF), Janus kinase 1 (JAK1), and signal transducer and activator of transcription 3 (STAT3) was increased, while that of suppressor of cytokine signaling 1 (SOCS1) was decreased in RIF patients. Growth hormone (GH) administration proved to have positive effects on embryo implantation in RIF patients, but the action mechanism of GH has not been elucidated yet. To this aim, we studied the effects of GH on the proliferation in vitro of endometrial adenocarcinoma Ishikawa cells. GH stimulated the expression of LIF and SOCS1, and through SOCS1 inhibits the expression of phosphorylated STAT3, and finally inhibits the occurrence of RIF. Excessive phosphorylation of STAT can lead to decreased endometrial receptivity and abnormal embryo implantation. We also examined the effects of LIF overexpression and an LIF inhibitor (EC330) on the JAK/STAT pathway. LIF promoted cell proliferation, and the up-regulation of LIF increased the expression of SOCS1 and JAK1/STAT3 pathway-related genes in Ishikawa cells. As GH can inhibit the JAK1/STAT3 pathway through LIF, we hypothesize that upregulating SOCS1 may be a potential approach to treat RIF at the molecular level. GH can inhibit the JAK1/STAT3 pathway through LIF, up-regulating SOCS1 to treat RIF at the molecular level.

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Effects of LncRNA Lnc-LIF-AS on cell proliferation, migration and invasion in a human cervical cancer cell line

Cited by 6 publications

References 42 publications

Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer

Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer

LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non‐small cell lung cancer cells via the miR‐361‐3p/FRAT1 axis

Growth hormone inhibits the JAK/STAT3 pathway by regulating SOCS1 in endometrial cells <em>in vitro</em>: a clue to enhance endometrial receptivity in recurrent implantation failure

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