LncRNA HEIH promotes cell proliferation, migration and invasion by suppressing miR-214-3p in gastric carcinoma

2020 ◽  
Author(s):  
Lei Jiang ◽  
Luyao Zhang ◽  
Qian Chen ◽  
Shigang Qiao ◽  
Feng Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Carcinoma ◽  
Quantitative Polymerase Chain Reaction ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Gastric Carcinoma Cell ◽  
Normal Tissues ◽  
Apoptosis Detection

Abstract The present study aimed to investigate the function of long non-coding RNA HEIH in gastric carcinoma (GC). Adjacent normal tissues and GC tissues were obtained from 72 patients. Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to measure the expression of HEIH in cancer tissues and cells. Cell Counting Kit-8 and transwell assays were employed to evaluate cell proliferation, migration and invasion. An Annexin V-fluorescein-isothiocyanate (FITC)/propidium iodide (PI) Apoptosis Detection Kit was used to evaluate the apoptosis ratio. RT-qPCR was used to detect the expression level of miR-214-3p. The expression of HEIH in GC tissues was higher than in adjacent normal tissues. The expression of HEIH was upregulated in MKN-45, NCL-N87, KATO III cell lines compared within normal gastric epithelial cells. Knockdown of lncRNA HEIH significantly decreased the number of migrated and invaded cells. Additionally, downregulation of HEIH could increase GC cell apoptosis compared with the non-specific control (NC) group. We also proved that miR-214-3p was the direct target of lncRNA HEIH, and that overexpression of miR-214-3p could reverse the effects of HEIH. Silencing of HEIH could suppress Gastric Carcinoma cell proliferation, migration and invasion by inhibiting miR-214-3p. Thus, HEIH might represent a novel biomarker and therapeutic target.

Tripterine inhibits proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating microRNA-15a

2019 ◽  
Vol 400 (8) ◽  
pp. 1069-1078 ◽  
Author(s):  
Anjun Zuo ◽  
Peng Zhao ◽  
Yu Zheng ◽  
Hui Hua ◽  
Xingang Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Annexin V ◽  
Cell Counting ◽  
Brdu Incorporation ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Apoptosis Detection ◽  
Incorporation Assay

Abstract Breast cancer is the most commonly diagnosed cancer in women worldwide. Tripterine is an important active component isolated from Triperygium wilfordii Hook F. This study investigated the effects of tripterine on breast cancer cell proliferation, migration, invasion and apoptosis, as well as microRNA-15a (miR-15a) expression. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to measure the expression of miR-15a. Cell transfection was conducted to change the expression of miR-15a. Viability, proliferation, migration, invasion and apoptosis of MDA-MB-231 cells were assessed using the cell counting kit-8 (CCK-8) assay, BrdU incorporation assay, Annexin V-FITC/PI apoptosis detection kit and two-chamber Transwell assay, respectively. Expression of key factors involving in cell proliferation, migration, invasion and apoptosis, as well as the PI3K/AKT and JNK pathways, were evaluated using Western blotting. We found that tripterine inhibited MDA-MB-231 cell viability, proliferation, migration and invasion, but induced cell apoptosis. Moreover, tripterine up-regulated the expression of miR-15a in a concentration-dependent manner and miR-15a participated in the effects of tripterine on MDA-MB-231 cell proliferation, migration, invasion and apoptosis. In addition, tripterine inactivated PI3K/AKT and JNK pathways in MDA-MB-231 cells by up-regulating miR-15a. In conclusion, tripterine inhibited proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating miR-15a and inactivating PI3K/AKT and JNK pathways.

scholarly journals CircHMGCS1 is upregulated in colorectal cancer and promotes proliferation of colorectal cancer cells by targeting microRNA-503-5p

2019 ◽  
Vol 17 ◽  
pp. 205873921986955 ◽  
Author(s):  
Jingqing Dong ◽  
Jun Li ◽  
Jihui Luo ◽  
Weiqiang Wu
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Clinical Parameter ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Apoptosis Pathway ◽  
Colorectal Cancer Cells ◽  
And Migration ◽  
Related Proteins

This study aims to explore the regulatory mechanism of circHMGCS1/microRNA-503-5p (miR-503-5p) axis during colorectal cancer (CRC) development and progression. Real-time quantitative polymerase chain reaction (RT-qPCR) was applied to evaluate the expression of circHMGCS1 and miR-503-5p in CRC samples and their adjacent non-tumor specimen. Then, cell proliferation and cell apoptosis and migration and invasion of circHMGCS1-knocked down cells were further detected, using cell counting kit-8 (CCK-8), flow cytometry, Transwell assay, and western blotting assays. CircHMGCS1 was found to be significantly upregulated in CRC, and its high expression was closely correlated with the poor clinical parameter. In addition, the knockdown of circHMGCS1 could significantly inhibit CRC cells’ growth promoting apoptosis, as suggested by the expression of apoptosis pathway-related proteins, which changed consistently. Furthermore, miR-503-5p inhibitors were able to reverse the suppression of cell proliferation induced by silencing circHMGCS1. Therefore, circHMGCS1 might serve as a promising bio-marker and treatment target for CRC.

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.

scholarly journals RNF43 Inhibits Cancer Cell Proliferation and Could be a Potential Prognostic Factor for Human Gastric Carcinoma

2015 ◽  
Vol 36 (5) ◽  
pp. 1835-1846 ◽  
Author(s):  
Lei Niu ◽  
Hong-Zhen Qin ◽  
Hong-Qing Xi ◽  
Bo Wei ◽  
Shao-You Xia ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Carcinoma ◽  
Tumor Formation ◽  
Cancer Prognosis ◽  
Depth Of Invasion ◽  
Regional Lymph Nodes ◽  
Gastric Carcinoma Cell ◽  
Normal Tissues ◽  
Gastric Carcinoma Cell Lines ◽  
Potential Prognostic Factor

Background/Aims: RNF43 is a member of transmembrane E3 ubiquitin ligases and plays important roles in tumor formation progression. In current study, we aimed to explore RNF43 expression and analyze its role in gastric carcinoma. Methods and Results: The level of RNF43 was detected in 77 cases of gastric carcinoma and matched normal tissues by real-time PCR, western blotting and immunohistochemistry. We found that the expression of RNF43 was significantly down-regulated in the gastric carcinoma tissues compared to the normal mucosae (all P<0.001). In addition, RNF43 was significantly correlated with histological differentiation (P = 0.001), T-stage cancer (P<0.001), depth of invasion (P<0.001), metastasis of regional lymph nodes (P<0.001), pTNM stage (P<0.001) and survival (P = 0.021). We further explored the biological functions of RNF43 in gastric carcinoma cell lines. Both gain- and loss-function assays show that RNF43 could suppress cell proliferation while promotes cell apoptosis. Further, we found that RNF43 was positively correlated with p53 and cleaved-caspase3 and negatively correlated with Ki67 and Lgr5. Concolusion: In conclusion, RNF43 might act as a tumor suppressor in gastric carcinoma and might be a potential indicator for the clinical assessment of gastric cancer prognosis

scholarly journals Exosomal circ_0088300 Derived From Cancer-Associated Fibroblasts Acts as a miR-1305 Sponge and Promotes Gastric Carcinoma Cell Tumorigenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Hao Shi ◽  
Shan Huang ◽  
Mingde Qin ◽  
Xiaofeng Xue ◽  
Xingpo Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Carcinoma ◽  
Carcinoma Cell ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Cancer Associated Fibroblasts ◽  
Regulatory Pathway ◽  
Gastric Carcinoma Cell ◽  
Cancer Associated Fibroblast ◽  
Potential Biomarker

Cancer-associated fibroblast (CAF)-derived exosomes play a major role in gastric carcinoma (GC) tumorigenesis. However, the mechanism behind the activity of circular RNAs in CAF-derived exosomes in GC remains unclear. In the present study, we identified differentially expressed circ_0088300 in GC tissues and plasma exosomes. We found that CAFs delivered functional circ_0088300 to GC tumor cells via exosomes and promoted the proliferation, migration and invasion abilities of GC cells. Furthermore, we demonstrated that circ_0088300 packaging into exosomes was driven by KHDRBS3. In addition, we verified that circ_0088300 served as a sponge that directly targeted miR-1305 and promoted GC cell proliferation, migration and invasion. Finally, the JAK/STAT signaling pathway was found to be involved in the circ_0088300/miR-1305 axis, which accelerates GC tumorigenesis. In conclusion, our results indicated a previously unknown regulatory pathway in which exosomal circ_0088300 derived from CAFs acts as a sponge of miR-1305 and promotes GC cell proliferation, migration and invasion; these data identify a potential biomarker and novel therapeutic target for GC in the future.

scholarly journals lncRNA LIFR‑AS1 inhibits gastric carcinoma cell proliferation, migration and invasion by sponging miR‑4698

2020 ◽  
Vol 23 (2) ◽  
Author(s):  
Jiangqiao Zhao ◽  
Xiaoning Li ◽  
Liping Fu ◽  
Na Zhang ◽  
Jiaping Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Carcinoma ◽  
Carcinoma Cell ◽  
Migration And Invasion ◽  
Gastric Carcinoma Cell

scholarly journals HOTAIR Promotes Cisplatin Resistance of Nasopharyngeal Carcinoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/SOX4 Axis

2020 ◽  
Author(s):  
Wei Cao ◽  
Yi Sun ◽  
Long Liu ◽  
Junwei Yu ◽  
Jiabiao Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Nasopharyngeal Carcinoma ◽  
Quantitative Polymerase Chain Reaction ◽  
Malignant Neoplasm ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Multi Drug Resistance ◽  
Migration And Invasion ◽  
Proliferation And Invasion

Abstract Background: Nasopharyngeal carcinoma (NPC) is a highly malignant neoplasm originating from nasopharyngeal mucosa, and the emergence of multi-drug resistance poses a huge challenge for clinical treatment of NPC. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including NPC. However, the underlying mechanisms of HOTAIR involved in drug resistance in NPC are obscure.Methods: Quantitative polymerase chain reaction (qPCR) was employed to determine the HOTAIR, miR-106a-5p and SOX4 expression in NPC tissues and cells. The target relationship between HOTAIR and miR-106a-5p or miR-106a-5p and SOX4 was determined using dual-luciferase reporter assay. Cell proliferation, apoptosis, migration and invasion were explored using Cell counting kit-8 (CCK-8), flow cytometer and Transwell assays. The protein levels were confirmed using western blot.Results: Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant NPC tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance related gene expression, cell proliferation and invasion, and promoted apoptosis of C666-1/DDP and CNE2/DDP cells. Mechanism researches displayed that miR-106a-5p was down-regulated in DDP-resistant NPC tissues and cells. miR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. SOX4 was inhibited by miR-106a-5p at a posttranscriptional level, and the transfection of miR-106a-5p reversed the upregulation of SOX4 caused by HOTAIR overexpression. Increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion and apoptosis of C666-1/DDP and CNE2/DDP cells. Moreover, the transfection of SOX4 siRNA reversed the decrease of DDP resistance, cell proliferation and invasion, and rescued the increase of apoptosis induced by miR-106a-5p inhibition. Conclusions: These data suggested that HOTAIR enhanced DDP resistance of C666-1/DDP and CNE2/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/SOX4 axis.

scholarly journals circ_0000467 promotes the proliferation, metastasis, and angiogenesis in colorectal cancer cells through regulating KLF12 expression by sponging miR-4766-5p

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1415-1427
Author(s):  
Hui Chen ◽  
Chen Wu ◽  
Liang Luo ◽  
Yuan Wang ◽  
Fangxing Peng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Reaction Cell ◽  
Western Blot Assay

Abstract Background Circular RNAs have been identified as crucial players in the initiation and progression of cancers, including colorectal cancer (CRC). The Has_circ_0000467 (circ_0000467) expression has been found to be upregulated in CRC, but its function and mechanism remain unclear. Methods The expression levels of circ_0000467, microRNA-4766-5p (miR-4766-5p), and Krueppel-like factor 12 (KLF12) were examined using reverse transcription-quantitative polymerase chain reaction. Cell proliferation was analyzed by cell counting kit-8 assay and colony formation assay. The apoptosis was measured by flow cytometry. Transwell migration and invasion assays were applied to evaluate cell metastatic ability. Angiogenesis was detected using tube formation assay. All protein expressions were quantified by western blot assay. Dual-luciferase reporter assay was used to analyze intergenic binding. Xenograft models were constructed for the experiment of circ_0000467 in vivo. Results The expression of circ_0000467 was upregulated in CRC tissues and cells. Knockdown of circ_0000467 repressed cell proliferation, metastasis, and angiogenesis, but it induced apoptosis in CRC cells. circ_0000467 targeted miR-4766-5p and inhibited the expression of miR-4766-5p. Silencing of circ_0000467 inhibited CRC progression by upregulating miR-4766-5p. miR-4766-5p suppressed the expression of target gene KLF12 and KLF12 overexpression reversed the effects of miR-4766-5p on CRC cell behaviors. circ_0000467 positively regulated the expression of KLF12 by targeting miR-4766-5p. circ_0000467 downregulation in vivo reduced CRC tumorigenesis by regulating miR-4766-5p and KLF12. Conclusion circ_0000467 acted as an oncogene in CRC through regulating KLF12 expression by sponging miR-4766-5p. Therefore, circ_0000467 can be used as an effective target in CRC diagnosis and therapy.

scholarly journals TRIM32 Promotes the Growth of Gastric Cancer Cells through Enhancing AKT Activity and Glucose Transportation

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Jianjun Wang ◽  
Yuejun Fang ◽  
Tao Liu
Keyword(s):  
Gastric Cancer ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Cell Counting ◽  
Akt Inhibitor ◽  
Gastric Cancer Cells ◽  
Poor Overall Survival ◽  
Reverse Transcription Pcr ◽  
Apoptosis Detection

Tripartite motif protein 32 (TRIM32), an E3 ubiquitin ligase, is a member of the TRIM protein family. However, the underlying function of TRIM32 in gastric cancer (GC) remains unclear. Here, we aimed to explore the function of TRIM32 in GC cells. TRIM32 was induced silencing and overexpression using RNA interference (RNAi) and lentiviral-mediate vector in GC cells, respectively. Moreover, the PI3K/AKT inhibitor LY294002 was used to examine the relationship between TRIM32 and AKT. Quantitative reverse-transcription PCR (qRT-PCR) and western blot were used to determine the mRNA and protein contents. The glucose analog 2-NBDG was used as a fluorescent probe for determining the activity of glucose transport. An annexin V-fluorescein isothiocyanate apoptosis detection kit was used to stain NCI-N87, MKN74, and MKN45 cells. Cell counting kit-8 (CCK-8) assay was used to examine cell proliferation. Our results indicated that TRIM32 was associated with poor overall survival of patients with GC. Moreover, TRIM32 was a proproliferation and antiapoptosis factor and involved in the AKT pathway in GC cells. Furthermore, TRIM32 possibly mediated the metabolism of glycolysis through targeting GLUT1 and HKII in GC cells. Importantly, TRIM32 silencing deeply suppressed the tumorigenicity of GC cells in vivo. Our findings not only enhanced the understanding of the function of TRIM32 but also indicated its potential value as a target in GC treatment.

scholarly journals MicroRNA-937 is overexpressed and predicts poor prognosis in patients with colon cancer

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Huiya Liu ◽  
Lin Ma ◽  
Ling Wang ◽  
Yizuo Yang
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cox Regression ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Prognostic Impact ◽  
Cancer Tissues

Abstract Background Colon cancer is a heterogeneous tumor and a leading cause of cancer-related mortality. MicroRNA (miRNA) has been proposed as the biomarker in cancers. The aim of this study was to investigate the clinical significance and potential functional role of miR-937 in colon cancer. Methods In the present study, reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was conducted to examine the expression levels of miR-937 in colon cancer tissues and cell lines. Kaplan-Meier curve and Cox regression analyses were used to determine the prognostic impact of miR-937 on survival. Cell Counting Kit-8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. Results miR-937 was significantly upregulated in colon cancer tissues and cell lines. Clinical analysis results showed that miR-937 expression was associated with lymph node metastasis and TNM stage. Patients with high miR-937 expression predicted a shorter overall survival rate. Functionally, overexpression of miR-937 promoted cell proliferation, migration, and invasion, while inhibition of miR-937 inhibited these cellular behaviors in vitro. Conclusions These results suggested that miR-937 may act as a prognostic biomarker and a potential target for therapeutic strategy, as well as promote proliferation, migration, and invasion of colon cancer.

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