scholarly journals LncRNA SLCO4A1-AS1 Accelerates Growth and Metastasis of Gastric Cancer via Regulation of the miR-149/XIAP Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Yantian Fang ◽  
Bo Sun ◽  
Jianpeng Gao ◽  
Yakai Huang ◽  
Chenchen Wang
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Advanced Tumor Stage ◽  
Xiap Expression ◽  
Mouse Xenograft Model ◽  
Tumor Growth And Metastasis

ObjectiveRecently, long noncoding RNA SLCO4A1 antisense RNA 1 (SLCO4A1-AS1) has been shown to act as an oncogene in several cancer types; however, its role in gastric cancer (GC) and its underlying molecular mechanisms are yet to be elucidated.MethodsUsing the ENCORI database, we identified SLCO4A1-AS1, miR-149-5p (miR-149), and the X-linked inhibitor of apoptosis (XIAP) whose expressions were obviously changed in GC samples, and analyzed the correlation between their expressions in GC samples. Moreover, we explored the expression of SLCO4A1-AS1, miR-149, and XIAP in clinical samples and GC cell lines using RT-qPCR and western blotting assay; the correlation between them was analyzed using RNA immunoprecipitation and dual-luciferase reporter. CCK-8, colony formation, and Transwell assays were conducted to determine the effects of SLCO4A1-AS1, miR-149, and XIAP expression on cell proliferation, migration, and invasion, respectively. A nude mouse xenograft model was used to explore their function in xenograft growth.ResultsSLCO4A1-AS1 was significantly upregulated in the GC samples and cell lines, and a high level of SLCO4A1-AS1 was associated with an advanced tumor stage and shortened patient survival. Mechanistically, SLCO4A1-AS1 post-transcriptionally regulated XIAP by functioning as competing endogenous RNA in GC to sponge miR-149. Further functional assays revealed that the overexpression of miR-149 and knockdown of XIAP considerably inhibited GC cell viability and its migratory and invasive characteristics in vitro. SLCO4A1-AS1 knockdown also determined the function of GC cells but was diminished by the miR-149 inhibitor in vitro. Finally, we demonstrated that the deletion of SLCO4A1-AS1 suppressed tumor growth and metastasis in vivo.ConclusionsAltogether, these findings suggest that SLCO4A1-AS1 functions as a crucial oncogenic lncRNA in GC and it can facilitate GC tumor growth and metastasis by interacting with miR-149 and enhancing XIAP expression. Therefore, SLCO4A1-AS1 is a potential novel therapeutic target in GC treatment.

scholarly journals miR-100-3p inhibits cell proliferation and induces apoptosis in human gastric cancer through targeting to BMPR2

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Chun-Wei Peng ◽  
Ling-Xiao Yue ◽  
Yuan-Qin Zhou ◽  
Sai Tang ◽  
Chen Kan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Over Expression ◽  
Qrt Pcr

Abstract Background miR-100 has been reported to closely associate with gastric cancer (GC) initiation and progression. However, the underlying mechanism of miR-100-3p in GC is still largely unclear. In this study, we intend to study how miR-100-3p regulates GC malignancy. Methods The expression levels of miR-100-3p in vitro (GES-1 and GC cell lines) and in vivo (cancerous and normal gastric tissues) were examined by quantitative real-time PCR (qRT-PCR). MTT and PE/Annexin V analyses were responsible for measurement of the effects of miR-100-3p on GC cell proliferation and apoptosis. Transwell assay with or without matrigel was used to examine the capacity of migration and invasion in GC cells. The interaction of miR-100-3p with bone morphogenetic protein receptor 2 (BMPR2) was confirmed through transcriptomics analysis and luciferase reporter assay. qRT-PCR and Western blot analyses were applied to determine the expression of ERK/AKT and Bax/Bcl2/Caspase3, which were responsible for the dysfunction of miR-100-3p. Results miR-100-3p was down-regulated in GC cell lines and cancerous tissues, and was negatively correlated with BMPR2. Loss of miR-100-3p promoted tumor growth and BMPR2 expression. Consistently, the effects of miR-100-3p inhibition on GC cells were partially neutralized by knockdown of BMPR2. Over-expression of miR-100-3p simultaneously inhibited tumor growth and down-regulated BMPR2 expression. Consistently, over-expression of BMPR2 partially neutralized the effects of miR-100-3p over-expression. Further study demonstrated that BMPR2 mediated the effects downstream of miR-100-3p, which might indirectly regulate ERK/AKT and Bax/Bcl2/Caspase3 signaling pathways. Conclusion miR-100-3p acted as a tumor-suppressor miRNA that down-regulated BMPR2, which consequently inhibited the ERK/AKT signaling and activated Bax/Bcl2/Caspase3 signaling. This finding provided novel insights into GC and could contribute to identify a new diagnostic and therapeutic target.

scholarly journals MiR-541-3p suppresses gastric cancer via negative regulation of HSF1

2021 ◽  
Vol 20 (11) ◽  
pp. 2293-2298
Author(s):  
Zihan Zheng ◽  
Peng Zhou ◽  
Yangyang Xiao ◽  
Qian Liu ◽  
Tao Wan
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Caspase 3 ◽  
Target Prediction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Microrna Target ◽  
Gastric Cancer Cells

Purpose: To explore the effects of miR-541-3P on the expression of heat shock transcription factor 1 (HSF1) in gastric cancer cells (GC).Methods: The MicroRNA Target Prediction Database was used to predict whether miR-541-3p interacts with HSF1. Interaction was assessed by dual-luciferase reporter assays. Furthermore, miR-541-3p mRNA levels in GC cell lines were determined by qRT-PCR. Human GC cell lines MKN45 and NCI-N87 were transfected with miR-541-3p mimic. Cell apoptosis, proliferation, invasion, and migration were evaluated using flow cytometry, apoptosis assays, Edu assays, CCK-8 assays, and transwell assays, respectively. Caspase-3, Bcl-2, and cleaved caspase-3 expression levels were determined by western blot.Results: Expression of miR-541-3p was significantly down-regulated in GC cells. Functionally, miR-541-3p mimic inhibited GC cell proliferation, migration, and invasion and induced apoptosis in vitro (p <0.01). Mechanistically, miR-541-3p interacted with HSF1 and inhibited its expression. Overexpression of HSF1 counteracted the effects of miR-541-3p mimic in GC cells.Conclusion: These results indicate that miR-541-3p suppresses the development of GC by targeting HSF1 and thus, is a possible strategy for for the management of GC.

scholarly journals LncRNA SNHG22 Sponges miR-128-3p to Promote Progression of Colorectal Cancer through Upregulating E2F3

2020 ◽  
Author(s):  
Yao Jianning ◽  
Wang Chunfeng ◽  
Dong Xuyang ◽  
Zhang Yanzhen ◽  
Li Yanle ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Mouse Xenograft Model ◽  
Mechanistic Investigation

Abstract Background: Long non-coding RNA (lncRNA) termed small nucleolar RNA host gene 22 (SNHG22) has been reported as a crucial regulator in several types of human cancers. In this study, we aimed to evaluate the function and mechanism of SNHG22 in colorectal cancer (CRC) progression. Methods: Quantitative RT-PCR (qRT-PCR) was used to detect the expression of SNHG22 in adenoma, tumor tissues (TTs), and adjacent nontumorous tissues (ANTs). The biological behaviors of SNHG22 in CRC cell lines were explored both in vitro (CCK-8 assay, flow cytometry, wound scratch, and transwell assays) and in vivo (nude mouse xenograft model). The interaction between SNHG22 and miR-128-3p, and the target genes of miR-128-3p were explored by online tools, qRT-PCR, western blot, and dual-luciferase reporter assay. Results: SNHG22 expression was gradually upregulated in ANTs, adenoma, and TTs. High expression levels of SNHG22 were significantly related to advanced clinicopathological factors and worse survival in patients with CRC. SNHG22 knockdown markedly prohibited CRC cell proliferation, migration, and invasion; and drove cell apoptosis in vitro; and hindered tumor growth in vivo. Mechanistic investigation showed that SNHG22 could bind to microRNA-128-3p (miR-128-3p) and attenuate its inhibitory effects on the expression levels and activity of E2F3. Rescue experiments exhibited that miR-128-3p inhibition or E2F3 upregulation can offset the functions of SNHG22 knockdown in CRC cells. Conclusion: Our findings support the existence of an interactive regulatory network of SNHG22, miR-128-3p, and E2F3 in CRC cell lines, indicating that the SNHG22/miR-128-3p/E2F3 axis is a novel diagnostic and therapeutic target in CRC.

MiR-4295 Promotes the Malignant Progression of Gastric Cancer via Targeting PTEN

2021 ◽  
Vol 25 ◽  
Author(s):  
Xiaoyan Yang ◽  
Jing Yang ◽  
Yunlian Tang ◽  
Zhizhong Xie ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Malignant Tumors ◽  
Mutual Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Cancer Tissues

Background: Gastric cancer (GC), one of the common clinical malignant tumors of the digestive system, is the fourth most commonly diagnosed cancer and the second lethal cancer worldwide, has the characteristics of high metastasis, fatality, and recurrence rate. This research was conducted to investigate the role and mechanism of miR-4295 in gastric cancer. Methods: The expression capacity of miR-4295 was determined in gastric cancer tissues and its normal tissues by qRT-PCR. PTEN expression level was detected by western blot. SGC-7901 and MGC-803 cell lines were cultured and transfected with miR-4295 or its inhibitor. The effects of miR-4295 on cell proliferation, colony formation, migration and invasion in vitro were investigated. The mutual effect between miR-4295 and PTEN in 293T cells was explored by luciferase reporter gene assays. Results: The results showed that miR-4295 expression was higher in gastric cancer tissues and cell lines, and the miR-4295 level was significantly negative associated with the tumor size and distal metastasis of gastric cancer. Notably, up-regulated miR-4295 promoted cell proliferation, migration and invasion in vitro, whereas it led to contrary effects while down-regulating miR-4295 expression. Further mechanism studies displayed that miR-4295 could directly fasten the PTEN 3’UTR and dramatically decrease the level of PTEN in vitro. Conclusion : The findings revealed that miR-4295 could promote gastric cancer cell proliferation, migration and invasion, which might be attributed to targeting PTEN. Our study suggested that miR-4295 might be a potential therapeutic target for gastric cancer.

scholarly journals A Novel lncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells

2020 ◽  
Author(s):  
cailin xue ◽  
xudong zhang ◽  
peng gao ◽  
weiwei yu ◽  
xiaohan cui ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Advanced Tumor Stage ◽  
Qrt Pcr ◽  
Advanced Tumor ◽  
Hcc Cells

Abstract Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, and has an unfavorable clinical outcome. Emerging evidences have demonstrated that long noncoding RNAs (lncRNAs) play an important role in the carcinogenesis and progression of HCC. However, the clinical significances, the biological roles of most lncRNAs in HCC remain poorly understood. Methods The expression levels of lncRNA loc339803 in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction(qRT-PCR) assay. The cellular sublocalization of loc339803 were determined by fluorescence in situ hybridization and nuclear & cytoplasmic RNA isolation assay. Western blot, CCK-8, Edu, colony formation, migration and invasion assays were used to investigate the roles of loc339803 in progression of HCC in vitro. A mouse model for lung metastasis was constructed to evaluate the role of loc339803 in HCC development in vivo. The correlations among loc339803, miR-30a-5p and SNAIL1 were validated by qRT-PCR and a dual- luciferase reporter assay. Results The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro. Further studies demonstrated the loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of snai1, a target gene of miR-30a-5p. Moreover, miR-30a-5p upregulation blocked the enhancement of migration and invasion of HCC cells induced by loc339803 overexpression. Conclusions Loc339803 may be oncogenic in HCC and associated with poor clinical outcomes. LncRNA loc339803 might promote the invasion and migration of HCC cells through regulating miR-30a-5p/ SNAIL1 axis.

scholarly journals HOXA-AS3 Promotes Proliferation and Migration of Hepatocellular Carcinoma Cells via the miR-455-5p/PD-L1 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Cheng Zeng ◽  
Shaojun Ye ◽  
Yu Chen ◽  
Qu Zhang ◽  
Yan Luo ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mouse Xenograft Model ◽  
Reporter Assays ◽  
Tumor Growth And Metastasis ◽  
And Migration ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) is the most prevalent type of hepatic carcinoma. Long noncoding RNAs (lncRNAs) are considered crucial regulators of gene expression; however, their functions in HCC are not well understood. Thus, the present study is aimed at elucidating the functions of the lncRNA HOXA-AS3 in HCC. The functions of the HOXA-AS3/miR-455-5p/programmed death-ligand 1 (PD-L1) axis were investigated in vitro via qRT-PCR and dual-luciferase reporter assays. The effect of HOXA-AS3 expression on tumor growth and metastasis was assessed using a mouse xenograft model. High HOXA-AS3 expression was observed in the HCC cell lines. Furthermore, overexpression of HOXA-AS3 in HCC cells enhanced proliferation, migration, and invasion, regulated the cell cycle, and retarded apoptosis. We also identified an miR-455-5p binding site in HOXA-AS3. By sponging miR-455-5p, HOXA-AS3 increased the expression of PD-L1. Additionally, both the inhibition of PD-L1 and overexpression of miR-455-5p reversed the effects on cell proliferation and invasion triggered by the overexpression of HOXA-AS3. In conclusion, HOXA-AS3 modulated the functions of HCC cells through the miR-455-5p/PD-L1 axis. Therefore, HOXA-AS3 may be a novel therapeutic target for HCC.

scholarly journals Identification of differentially expressed circRNAs and a novel hsa_circ_0000144 that promote tumor growth in gastric cancer

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jianming Wei ◽  
Jinmiao Wang ◽  
Xibo Gao ◽  
Feng Qi
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Regulatory Network ◽  
Differentially Expressed ◽  
Migration And Invasion ◽  
Pathway Network

Abstract Background Circular RNAs (circRNAs) are involved in regulating tumor pathogenesis. The mechanism of circRNAs in gastric cancer (GC) is still unknown. Our study aimed to identify differentially expressed circRNAs and assess a novel circRNA (hsa_circ_0000144) in the proliferation, migration, and invasion in GC. Methods Gene ontology (GO) enrichment and analyses of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, pathway network, and the ceRNA regulatory network of hsa_circ_0000144 targeting miRNAs and mRNAs were performed with the help of bioinformatics using R language and Perl software. hsa_circ_0000144 expression and circRNA knockdown in GC cell lines were detected using quantitative PCR (qPCR) in vitro. Cell proliferation, migration, and invasion after circRNA knockdown were measured using the cell counting kit-8 assay and Transwell assay. Results The circRNA expression profile GSE78092 downloaded from the Gene Expression Omnibus database included three GC patients and three normal tissues. Thirty-two differentially expressed circRNAs comprised six upregulated circRNAs and 26 downregulated circRNAs. In particular, the ErbB signaling pathway, neurotrophin signaling pathway, cellular senescence, and pathways in bladder cancer and GC played the most important roles in the pathway network. The expression of hsa_circ_0000144 was upregulated in GC cell lines. Hsa_circ_0000144 knockdown suppressed tumor growth in vitro. Conclusions Hsa_circ_0000144 promotes GC cell proliferation, migration, and invasion, and the ceRNA regulatory network of hsa_circ_0000144 targeting miRNAs and mRNAs might be biomarkers for GC diagnosis and targeted therapy.

scholarly journals Activation of the KDM5A/miRNA-495/YTHDF2/m6A-MOB3B axis facilitates prostate cancer progression

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Chen Du ◽  
Caihong Lv ◽  
Yue Feng ◽  
Siwen Yu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cell Lines ◽  
Cancer Progression ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Accumulating evidence supports that lysine-specific demethylase 5 (KDM5) family members act as oncogenic drivers. This study was performed to elucidate the potential effects of KDM5A on prostate cancer (PCa) progression via the miR-495/YTHDF2/m6A-MOB3B axis. Methods The expression of KDM5A, miR-495, YTHDF2 and MOB3B was validated in human PCa tissues and cell lines. Ectopic expression and knockdown experiments were developed in PCa cells to evaluate their effects on PCa cell proliferation, migration, invasion and apoptosis. Mechanistic insights into the interaction among KDM5A, miR-495, YTHDF2 and MOB3B were obtained after dual luciferase reporter, ChIP, and PAR-CLIP assays. Me-RIP assay was used to determine m6A modification level of MOB3B mRNA in PCa cells. Mouse xenograft models of PCa cells were also established to monitor the tumor growth. Results KDM5A was highly expressed in human PCa tissues and cell lines. Upregulated KDM5A stimulated PCa cell proliferation, migration and invasion, but reduced cell apoptosis. Mechanistically, KDM5A, as a H3K4me3 demethylase, bound to the miR-495 promoter, which led to inhibition of its transcription and expression. As a target of miR-495, YTHDF2 could inhibit MOB3B expression by recognizing m6A modification of MOB3B mRNA and inducing mRNA degradation. Furthermore, KDM5A was found to downregulate MOB3B expression, consequently augmenting PCa cell proliferation, migration and invasion in vitro and promoting tumor growth in vivo via the miR-495/YTHDF2 axis. Conclusion In summary, our study highlights the potential of histone demethylase KDM5A activity in enhancing PCa progression, and suggests KDM5A as a promising target for PCa treatment.

scholarly journals Downregulation of long noncoding RNA LINC01419 inhibits cell migration, invasion, and tumor growth and promotes autophagy via inactivation of the PI3K/Akt1/mTOR pathway in gastric cancer

2019 ◽  
Vol 11 ◽  
pp. 175883591987465 ◽  
Author(s):  
Lin-Lin Wang ◽  
Lei Zhang ◽  
Xiao-Feng Cui
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Noncoding Rna ◽  
Mtor Pathway ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tumor Growth And Metastasis

Background: Accumulating evidence has highlighted the crucial role of long noncoding RNAs (lncRNAs) in the tumorigenesis of gastric cancer (GC), which is the most common gastrointestinal malignancy. The present study aimed to identify the capacity of lncRNA LINC01419 (LINC01419) in GC progression, with the potential mechanism explored. Methods: Highly expressed lncRNAs were identified by in silico analysis, with the LINC01419 expression in GC tissues measured using reverse transcription-quantitative PCR (RT-qPCR). The GC cells were subsequently transfected with siRNA against LINC01419 or Rapamycin (the inhibitor of the mTOR pathway), or both, in order to measure cell migration and invasion in vitro as well as tumor growth and metastasis in vivo. Moreover, the expression of PI3K/Akt1/mTOR pathway-associated factors was determined. Results: LINC01419, highly expressed in GC samples of the Gene Expression Omnibus database, was observed to be markedly upregulated in GC tissues. Moreover, LINC01419 silencing, or PI3K/Akt1/mTOR pathway inhibition, exhibited an inhibitory role in GC cell migration and invasion in vitro, coupled with promoted cell autophagy in vitro, and inhibited tumor growth and metastasis in vivo. It was also revealed that LINC01419 silencing blocked the PI3K/Akt1/mTOR pathway, as proved by decreased extents of Akt1 and mTOR phosphorylation. Conclusions: In conclusion, LINC01419 inhibition may suppress GC cell invasion and migration, and promote autophagy via inhibition of the PI3K/Akt1/mTOR pathway. This provides significant theoretical basis and possibilities for further elucidation of the molecular mechanism of GC and finding new molecular-targeted therapeutic regimens.

scholarly journals Downregulation of LANCL1-AS1 Promotes Tumorigenesis in Lung Adenocarcinoma Via the Modulation of miR-6748a-3p/PRSS8 Axis

2021 ◽  
Author(s):  
Guangjie Nie ◽  
Jun Liu ◽  
Jiakang Liang ◽  
Yi Yuan
Keyword(s):  
Protein Expression ◽  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Tissue Samples ◽  
Proliferation Capacity

Abstract Background: Lung adenocarcinoma (LUAD) is one of the deadliest types of cancer worldwide. Previous studies have reported that the expression of LANCL1-AS1 was decreased in LUAD. Hence, the current study was conducted to confirm these findings and explore the probable mechanism of action.Methods: LUAD and adjacent tissue samples were collected after the surgical procedure. For experiments in vitro, CCK-8 assay and colony formation assay were employed to explore the proliferation capacity while transwell assay was performed to explore the migration and invasion ability of LUAD cell lines. Luciferase reporter assay and RNA pull-down assay were used to confirm the interaction between LANCL1-AS1 and corresponding miRNA as well as the corresponding protein target of the miRNA predicted by online bioinformatics tools. The effect of different interventions on RNA and protein expression was confirmed by qRT-PCR and western blotting.Results: It was observed that LANCL1-AS1 was low expressed in LUAD tissues and cell lines which was also associated with decreased survival of cancer patients. Overexpression of LANCL1-AS1 in cell lines was associated with decreased viability, proliferation, migration, and invasion, and with decreased subcutaneous tumor growth in nude mice. RNA pull-down and luciferase reporter gene assays suggested that LANCL1-AS1 interacted with miR-6748a-3p and LUAD tissue samples exhibited increased expression of miR-6748a-3p. Moreover, miR-6748-3p mimics decreased the RNA and protein expression of PRSS8 in LUAD cell lines. Interestingly, LUAD tissue samples exhibited low expression of PRSS8. The effects of LANCL1-AS1 overexpression on viability, proliferation, migration, and invasion capacity of LUAD cell lines were curtailed after the miR-6748a-3p overexpression or PRSS8 silencing. Conclusion: Our results suggest that upregulation of LANCL1-AS1 can suppress tumor growth in LUAD through the modulation of miR-6748a-3p and PRSS8 dependent pathways.

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