scholarly journals LINC01128 expedites cervical cancer progression by regulating miR-383-5p/SFN axis

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yi Hu ◽  
Yan Ma ◽  
Jie Liu ◽  
Yanlin Cai ◽  
Mengmeng Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Cell Apoptosis ◽  
High Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Real Time Quantitative Pcr ◽  
Protein Levels ◽  
Normal Tissues

Abstract Background Cervical cancer (CC), causing significant morbidity and mortality worldwide, is one of the most common gynecological malignancies in women. SFN has been reported as a potential prognostic marker with apparent high expression in tumors. Nevertheless, the function mechanism of SFN is not clear yet in CC. Methods The relative expressions of RNAs were detected by real-time quantitative PCR (RT-qPCR). Colony formation assay, EdU stained assay and CCK-8 assay were to check cell proliferation ability in CC. Flow cytometry and apoptosis related proteins analysis were used to measure cells apoptosis capacity. Luciferase reporter assay and RNA pull down assay were to verify the molecular mechanism. Results SFN was highly expressed in CC tissues and CC cell lines compared with normal tissues and normal cell line. After interfering SFN, cell proliferation, migration and invasion ability was inhibited as well as cell apoptosis ability was promoted. In subsequence, miR-383-5p exhibited conspicuous low expression in CC tissues. And miR-383-5p was found to bind to SFN and have anti-cancerous effects in CC. Moreover, LINC01128 displayed remarkable high expression in CC tissues. Besides, LINC01128 shortage could reduce the expression of SFN at mRNA and protein levels. And the affinity between LINC01128 and miR-383-5p was verified. In the end, it was proved that LINC01128 could enhance cell proliferation, migration and invasion as well as inhibit cell apoptosis by binding with miR-383-5p and upregulating SFN. Conclusion LINC01128 expedited cells cellular process in CC by binding with miR-383-5p to release SFN. Graphical Abstract

scholarly journals Circ-CCDC66 Upregulates REXO1 Expression to Aggravate Cervical Cancer Progression Via Restraining miR-452-5p

2020 ◽  
Author(s):  
Yun Zhang ◽  
Xing Li ◽  
Jun Zhang ◽  
Lin Mao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Model ◽  
Tumor Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Fractionation ◽  
Real Time Quantitative Pcr ◽  
Cancer Tumor

Abstract BackgroundCervical cancer is one most common cancer types among females around the world. CircRNAs have been revealed to participate in multiple biological functions, and are involved in many diseases’ progression. In current study, we aimed to elucidate whether circ-CCDC66 participates cervical cancer progression. MethodsReal-time quantitative PCR (RT-qPCR) was conducted to measure the expression of circ-CCDC66, miR-452-5p, and REXO1 mRNA. Cell fractionation assay and RNA fluorescence in situ hybridization (FISH) were performed to locate circ-CCDC66 in cells. Cell proliferation ability was detected using cell account kit 8 (CCK-8). TRANSWELL assay was applied to evaluate cell migration or invasion ability. Bioinformatics analysis, biotinylated RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assays were conducted to assess the association between miR-452 and circ-CCDC66 or REXO1. Western blot was applied to measure the protein expression of REXO1. Animal tumor model was used to assess the effect of circ-CCDC66 in vivo.ResultsCirc-CCDC66 was upregulated in cervical cancer tumor tissues, and correlated with tumor stage and tumor size. Downregulation of circ-CCDC66 inhibited cervical cancer cell proliferation, migration, and invasion. Circ-CCDC66 was an efficient molecular sponge for miR-452-5p, and negatively regulated miR-452-5p expression. MiR-452 directly targeted REXO1. The effects of circ-CCDC66 on cervical cancer cells were functioned through miR-452-5p/REXO1 axis. In animal experiment, downregulation of circ-CCDC66 was found to suppress tumor growth in vivo.ConclusionOur results demonstrated the effects of circ-CCDC66/miR-452-5p/REXO1 axis in cervical cancer progression, we might provide a novel therapeutic target for cervical cancer.

scholarly journals CircRNA8924 Promotes Cervical Cancer Cell Proliferation, Migration and Invasion by Competitively Binding to MiR-518d-5p /519-5p Family and Modulating the Expression of CBX8

2018 ◽  
Vol 48 (1) ◽  
pp. 173-184 ◽  
Author(s):  
Jiamei Liu ◽  
Danbo Wang ◽  
Zaiqiu Long ◽  
Jing Liu ◽  
Weishan Li
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Myometrial Invasion ◽  
Expression Level ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Normal Tissues

Background/Aims: Circular RNAs (circRNAs) play a significant role in the development and progression of various human cancers. However, the expression and function of circRNAs in cervical cancer (CC) have rarely been explored. The aim of this study was to investigate the biological function of circRNA8924 in CC and elucidate the possible molecular mechanism involved. Methods: Quantitative polymerase chain reaction was used to determine mRNA expression of circRNA8924, miR-518d-5p/519-5p and CBX8 in CC tissues and cells. CBX8 protein expression was measured by Western blotting. The CCK-8 assay was used to evaluate cell proliferation, and the transwell assay to determine cell migration and invasion. The luciferase reporter assay was used to determine the direct regulation of miR-518d-5p/519-5p and circRNA8924 or CBX8 Results: The study demonstrated that the expression level of circRNA8924 in CC was significantly higher than that in the adjacent normal tissues (P < 0.001), and that it was also associated with tumor size, FIGO staging and myometrial invasion. The knockdown of circRNA8924 significantly inhibited the proliferation, migration and invasion of CC cells SiHa and HeLa. The expression level of miR-518d-5p/519-5p was negatively correlated with circRNA8924, and circRNA8924 regulated CBX8 by competitively binding to miR-518d-5p/519-5p. Conclusions: CircRNA8924 is highly expressed in CC tissue and can be considered a competitive endogenous RNA of the miR-518d-5p/519-5p family to promote the malignant biological behavior of CC cells. It is suggested that it may serve as a new biomarker for CC diagnosis and disease progression and provide potential targets for targeted therapy.

MiR-302a-3p, Sponged by HOXA-AS2, Suppresses Cell Proliferation and Invasion in Lung Cancer Cells

2019 ◽  
Vol 9 (12) ◽  
pp. 1644-1652
Author(s):  
Xueqin Pan ◽  
Dongchun Ma
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cell Apoptosis ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion

Lung cancer is one of the most common malignant cancers with a poor survival rate and high mortality worldwide. MiRNAs have been evaluated as crucial regulators of human gene expression, and exerted vital role involved in cancer progression. MiR-302a-3p was aberrant expressed in cancers that include pancreatic cancer and hepatocellular cancer, but its biological role in lung cancer remains elusive. This study aimed to discover the role and potential mechanism of miR-302a-3p in lung cancer. The lung cancer cell line with the highest expression of miR-302a-3p was selected, which was then subjected to transfection of miR-302a-3p mimic. Quantitative RT-PCR was performed to detect gene expression. Western blot assay was performed to determine corresponding genes that related to cell proliferation, apoptosis and invasion. Cell Counting Kit (CCK)-8 assay, flow cytometry analysis, wound healing and Transwell assay were performed to detect cell proliferation, apoptosis, migration and invasion, respectively. Luciferase reporter assay was carried out to identify the targeting relationship of miR-302-3p and HOXA-AS2. MiR-302a-3p was downregulated in lung cancer cells, and overexpression of miR-302a-3p significantly suppressed cell proliferation, migration, invasion and promoted cell apoptosis. HOXA-AS2 was a direct target of miR-302a-3p and was regulated by miR-302a-3p. HOXA-AS2 was upregulated in lung cancer cells. Upregulated HOXA-AS2 could reverse the effect that overexpression of miR-302a-3p caused on cell proliferation, apoptosis, migration and invasion. Overall, miR-302a-3p exhibited anti-oncogenic activity by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis in lung cancer by targeting HOXA-AS2, disclosing the role and regulatory mechanism of miR-302a-3p, which provided a promising therapeutic target for the clinical application of lung cancer treatment.

scholarly journals Circ-CCDC66 upregulates REXO1 expression to aggravate cervical cancer progression via restraining miR-452-5p

2020 ◽  
Author(s):  
Yan Zhang ◽  
Xing Li ◽  
Jun Zhang ◽  
Lin Mao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Model ◽  
Tumor Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Fractionation

Abstract Background: Cervical cancer is one most common cancer types among females over the world. While its underlying mechanisms remain unclear. Circ-CCDC66 has been revealed to participate in multiple biological functions, and contribute to various diseases’ progression. In the current study, we aimed to demonstrate the role of circ-CCDC66 in cervical cancer progression. Methods: Real-time quantitative PCR (RT-qPCR) was conducted to measure the expression of circ-CCDC66, miR-452-5p, and REXO1 mRNA. Cell fractionation assay and RNA fluorescence in situ hybridization (FISH) were performed to locate circ-CCDC66 in cells. Cell account kit 8 (CCK-8) was used to detect cell proliferation ability. Transwell assay was applied to evaluate cell migration or invasion ability. Bioinformatics analysis, biotinylated RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assays were conducted to assess the association between miR-452 and circ-CCDC66 or REXO1. Western blot was applied to measure the protein expression of REXO1. The animal tumor model was used to assess the effect of circ-CCDC66 in vivo . Results: The expression of circ-CCDC66 was upregulated in cervical cancer tumor tissues in comparison with normal tissues, and correlated with later tumor stage and larger tumor size. Downregulated circ-CCDC66 inhibited cervical cancer cell proliferation, migration, and invasion. Circ-CCDC66 was an efficient molecular sponge for miR-452-5p, and negatively regulated miR-452-5p expression. MiR-452-5p directly targeted to REXO1. Circ-CCDC66 regulated REXO1 expression to modulate cervical cancer progression via miR-452-5p. Moreover, downregulated circ-CCDC66 was found to suppress tumor growth in vivo. Conclusion: Our results demonstrated the role of circ-CCDC66/miR-452-5p/REXO1 axis in cervical cancer progression, we might provide novel therapeutic targets for cervical cancer clinical intervention.

scholarly journals miR-654-5p promotes gastric cancer progression via the GPRIN1/NF-κB pathway

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1683-1695
Author(s):  
Weidong Zhou ◽  
Peifei Li ◽  
Peihua Jin
Keyword(s):  
Cell Proliferation ◽  
Cancer Progression ◽  
Binding Capacity ◽  
Quantitative Polymerase Chain Reaction ◽  
Malignant Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Inhibitory Influence ◽  
Protein Levels ◽  
Incidence And Mortality

Abstract Background Gastric carcinoma (GC) ranks the fifth most common cancer worldwide, with high incidence and mortality rates. Numerous microRNAs (miRNAs), including miR-654-5p, have been implicated in the pathophysiological processes of tumorigenesis. Nevertheless, the mechanism of miR-654-5p in GC is unclear. Objectives Our study is devoted to exploring the function and molecular mechanism of miR-654-5p on the malignant cell behaviors of GC. Methods The gene expression was detected by reverse transcription quantitative polymerase chain reaction. GC cell proliferation and motion were assessed by colony formation assay and transwell assay. The binding capacity between miR-654-5p and G protein-regulated inducer of neurite outgrowth 1 (GPRIN1) was explored by luciferase reporter and RNA pulldown assays. The protein levels were detected by Western blotting. Results miR-654-5p expression was higher in GC cells and tissues than control cells and tissues. miR-654-5p promoted GC cell growth and motion. Moreover, our findings showed that miR-654-5p was bound with GPRIN1. Importantly, downregulation of GPRIN1 rescued the inhibitory influence of miR-654-5p knockdown on GC cell malignant behaviors. Additionally, miR-654-5p activated the nuclear factor kappa-B (NF-κB) pathway by regulation of GPRIN1. Conclusions miR-654-5p facilitated cell proliferation, migration, and invasion in GC via targeting the GPRIN1 to activate the NF-κB pathway.

scholarly journals The novel circCLK3/miR-320a/FoxM1 axis promotes cervical cancer progression

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Hanqing Hong ◽  
Hai Zhu ◽  
Shujun Zhao ◽  
Kaili Wang ◽  
Nan Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Normal Tissues ◽  
Cancer Tissues

AbstractAs a new class of non-coding RNA, circular RNAs (circRNAs) play crucial roles in the development and progression of various cancers. However, the detailed functions of circRNAs in cervical cancer have seldom been reported. In this study, circRNA sequence was applied to detect the differentially expressed circRNAs between cervical cancer tissues and adjacent normal tissues. The relationships between circCLK3 level with clinicopathological characteristics and prognosis were analyzed. In vitro CCK-8, cell count, cell colony, cell wound healing, transwell migration and invasion, and in vivo tumorigenesis and lung metastasis models were performed to evaluate the functions of circCLK3. The pull-down, RNA immunoprecipitation (RIP), luciferase reporter and rescue assays were employed to clarify the interaction between circCLK3 and miR-320a and the regulation of miR-320a on FoxM1. We found that the level of circCLK3 was remarkably higher in cervical cancer tissues than in adjacent normal tissues, and closely associated with tumor differentiation, FIGO stage and depth of stromal invasion. Down-regulated circCLK3 evidently inhibited cell growth and metastasis of cervical cancer in vitro and in vivo, while up-regulated circCLK3 significantly promoted cell growth and metastasis in vitro and in vivo. The pull-down, luciferase reporter and RIP assays demonstrated that circCLK3 directly bound to and sponge miR-320a. MiR-320a suppressed the expression of FoxM1 through directly binding to 3′UTR of FoxM1 mRNA. In addition, FoxM1 promoted cell proliferation, migration, and invasion of cervical cancer, while miR-320a suppressed cell proliferation, migration, and invasion through suppressing FoxM1, and circCLK3 enhanced cell proliferation, migration and invasion through sponging miR-320a and promoting FoxM1 expression. In summary, circCLK3 may serve as a novel diagnostic biomarker for disease progression and a promising molecular target for early diagnoses and treatments of cervical cancer.

scholarly journals MiR-132-3p suppresses cell proliferation and migration in gastric cancer by targeting KIF21B/Wnt/β-catenin signaling pathway

2021 ◽  
Author(s):  
Bingtian Liu ◽  
Ling Qiang ◽  
Bingxin Guan ◽  
Zhipeng Ji
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Functional Role ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Microarray Gene Expression ◽  
Protein Levels ◽  
Normal Tissues ◽  
And Migration

Abstract Background: Recently, kinesin family member 21B (KIF21B) has been reported to be an oncogene in non-small cell lung cancer and hepatocellular carcinoma. However, the functional role and related molecular mechanisms underlying gastric cancer (GC) pathogenesis remain largely uncovered. Methods: The expression of KIF21B was investigated by analysis of Oncomine microarray gene expression datasets and clinical specimens. The association between KIF21B and miR-132-3p was assessed by luciferase reporter assay. CCK-8 assay and transwell assay were performed to analyze the functional role of miR-132-3p/KIF21B in GC cells. Related protein expression levels were evaluated by immunohistochemistry and western blot analysis.Results: We first found that the expression of KIF21B was upregulated in GC tissues compared with adjunct normal tissues. Knockdown of KIF21B significantly suppressed the proliferation, migration and invasion in GC cell lines (AGS and SNU-5). KIF21B was confirmed as the target of miR-132-3p in GC cells. Moreover, miR-132-3p was down-regulated and inversely correlated with KIF21B expression in GC tissues. Further functional experiments demonstrated that overexpression of KIF21B remarkedly reversed the suppressive effects of miR-132-3p overexpression on GC cell proliferation, migration and invasion. Furthermore, miR-132-3p overexpression downregulated the protein levels of Wnt1, c-Myc, β-catenin, PCNA and N-cadherin, and upregulated E-cadherin expression in GC cells, which were all alleviated after KIF21B overexpression. Conclusions: In summary, our findings provide the first evidence that down-regulation of KIF21B by miR-132-3p suppresses cellular functions in GC via regulating Wnt/β-catenin signaling.

scholarly journals Effect of microRNA-135a on Cell Proliferation, Migration, Invasion, Apoptosis and Tumor Angiogenesis Through the IGF-1/PI3K/Akt Signaling Pathway in Non-Small Cell Lung Cancer

2017 ◽  
Vol 42 (4) ◽  
pp. 1431-1446 ◽  
Author(s):  
Yufei Zhou ◽  
Shaoxia Li ◽  
Jiangtao Li ◽  
Dongfeng Wang ◽  
Quanxing Li
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Tumor Angiogenesis ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
Protein Levels ◽  
Normal Tissues

Objective: This study explored the ability of microRNA-135a (miR-135a) to influence cell proliferation, migration, invasion, apoptosis and tumor angiogenesis through the IGF-1/PI3K/Akt signaling pathway in non-small cell lung cancer (NSCLC). Methods: NSCLC tissues and adjacent normal tissues were collected from 138 NSCLC patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-135a and IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 mRNA; western blotting was used to determine the expression levels of IGF-1, PI3K and Akt protein; and enzyme-linked immunosorbent assay (ELISA) was used to analyze the expression levels of VEGF, bFGF and IL-8 protein. Human NSCLC cell lines (A549, H460, and H1299) and the human bronchial epithelial cell line (HBE) were selected. A549 cells were assigned to blank, negative control (NC), miR-135a mimics, miR-135a inhibitors, IGF-1 siRNA and miR-135a inhibitors + IGF-1 siRNA groups. The following were performed: an MTT assay to assess cell proliferation, a scratch test to detect cell migration, a Transwell assay to measure cell invasion, and a flow cytometry to analyze cell apoptosis. Results: The expression level of miR-135a was lower while those of IGF-1, PI3K and Akt mRNA were higher in NSCLC tissues than in the adjacent normal tissues. Dual-luciferase reporter assay indicated IGF-1 as a target of miR-135a. The in vitro results showed that compared with the blank group, cell proliferation, migration and invasion were suppressed, mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 were reduced, and cell apoptosis was enhanced in the miR-135a mimics and IGF-1 siRNA groups. Compared with the IGF-1 siRNA group, cells in the miR-135a inhibitors + IGF-1 siRNA group demonstrated increased cell proliferation, migration and invasion, elevated mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 and reduced cell apoptosis. Conclusion: These findings indicated that miR-135a promotes cell apoptosis and inhibits cell proliferation, migration, invasion and tumor angiogenesis by targeting IGF-1 gene through the IGF-1/PI3K/Akt signaling pathway in NSCLC.

scholarly journals Circ-CCDC66 upregulates REXO1 expression to aggravate cervical cancer progression via restraining miR-452-5p

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yan Zhang ◽  
Xing Li ◽  
Jun Zhang ◽  
Lin Mao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Tumor Model ◽  
Tumor Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Fractionation

Abstract Background Cervical cancer is one most common cancer types among females over the world. While its underlying mechanisms remain unclear. Circ-CCDC66 has been revealed to participate in multiple biological functions, and contribute to various diseases’ progression. In the current study, we aimed to demonstrate the role of circ-CCDC66 in cervical cancer progression. Methods Real-time quantitative PCR (RT-qPCR) was conducted to measure the expression of circ-CCDC66, miR-452-5p, and REXO1 mRNA. Cell fractionation assay and RNA fluorescence in situ hybridization (FISH) were performed to locate circ-CCDC66 in cells. Cell account kit 8 (CCK-8) was used to detect cell proliferation ability. Transwell assay was applied to evaluate cell migration or invasion ability. Bioinformatics analysis, biotinylated RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assays were conducted to assess the association between miR-452 and circ-CCDC66 or REXO1. Western blot was applied to measure the protein expression of REXO1. The animal tumor model was used to assess the effect of circ-CCDC66 in vivo. Results The expression of circ-CCDC66 was upregulated in cervical cancer tumor tissues in comparison with normal tissues, and correlated with later tumor stage and larger tumor size. Downregulated circ-CCDC66 inhibited cervical cancer cell proliferation, migration, and invasion. Circ-CCDC66 was an efficient molecular sponge for miR-452-5p, and negatively regulated miR-452-5p expression. MiR-452-5p directly targeted to REXO1. Circ-CCDC66 regulated REXO1 expression to modulate cervical cancer progression via miR-452-5p. Moreover, downregulated circ-CCDC66 was found to suppress tumor growth in vivo. Conclusion Our results demonstrated the role of circ-CCDC66/miR-452-5p/REXO1 axis in cervical cancer progression, we might provide novel therapeutic targets for cervical cancer clinical intervention.

LncRNA LINC00858 enhances cervical cancer cell growth through miR-3064-5p/ VMA21 axis

2021 ◽  
pp. 1-11
Author(s):  
Min Wei ◽  
Youguo Chen ◽  
Wensheng Du
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Cancer Cell Growth ◽  
Protein Coding ◽  
Gynecological Malignancy ◽  
Promising Therapeutic Target ◽  
Proliferation And Apoptosis ◽  
Reporter Assays

BACKGROUND: Cervical cancer (CC) is the most common form of gynecological malignancy. Long intergenic non-protein coding RNA 858 (LINC00858) has been identified to participate in multiple cancers. However, the role and mechanism of LINC00858 in CC cells are still elusive. AIM: The aim of this study is to explore the biological functions and mechanisms of LINC00858 in CC cells. METHODS: RT-qPCR analysis was used to examine the expression of LINC00858 in CC cells. EdU and colony formation assay were utilized to assess cell proliferation. TUNEL assay and flow cytometry assay were conducted to assess cell apoptosis. The mechanism regarding LINC00858 was certified through RNA pull down, RIP and luciferase reporter assays. RESULTS: The up-regulated LINC00858 was detected in CC cells. Reduction of LINC00858 effectively subdued CC cells proliferation and stimulated cell apoptosis. LINC00858 was determined to bind with miR-3064-5p and up-regulate VMA21 in CC cells. In rescue assays, miR-3064-5p down-regulation and VMA21 up-regulation were able to counteract the effect caused by LINC00858 decrease on CC cell proliferation and apoptosis. CONCLUSION: LINC00858 enhances cell proliferation, while restraining cell apoptosis in CC through targeting miR-3064-5p/VMA21 axis, implying that LINC00858 may serve as a promising therapeutic target for CC.

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