Long Non-Coding RNA Small Nucleolar RNA Host Gene 1 and MicroRNA-100-3p Expression in Endometrial Carcinoma and Its Effect on the Proliferation and Apoptosis of Ishikawa Cells

2021 ◽  
Vol 11 (6) ◽  
pp. 1046-1052
Author(s):  
Jiana Mao ◽  
Yulan Liu ◽  
Cainuo Shen ◽  
Xiaoxia Duan ◽  
Yier Chen
Keyword(s):  
Endometrial Cancer ◽  
Cell Viability ◽  
Caspase 3 ◽  
Pcr Assay ◽  
Cell Ratio ◽  
Apoptosis Rate ◽  
Qrt Pcr ◽  
Proliferation And Apoptosis ◽  
Ishikawa Cells ◽  
Cancer Tissues

The aim of this study was to explore LncRNA SNHG1 and miRNA-100-3p expression in endometrial carcinoma and its effect on the proliferation and apoptosis of Ishikawa cells. A qRT-PCR assay was conducted to determine SNHG1 and miRNA-100-3p expression in endometrial cancer tissues and paracancerous tissues. Human endometrial cancer Ishikawa cells were cultured in vitro. Si-NC, si-SNHG1, si-SNHG1, anti-miRNA-NC, and si-SNHG1 were transfected into Ishikawa cells with anti-miRNA-519b-3p. A qRT-PCR assay was performed to determine SNHG1 and miRNA-100-3p expression, and the CCK-8 method was used to determine cell proliferation. Flow cytometry was conducted to determine cell cycle and apoptosis rate and a dualluciferase reporter experiment was carried out to test the targeting association between SNHG1 and miRNA-100-3p. Cleave Caspase-3, CHOP, and ATF4 expression were determined with the Western Blot method. SNHG1 expression level and miRNA-519b-3p expression level were much higher and much lower, respectively, in endometrial cancer tissues than in paracancerous tissues (P < 0.05). Transfection of si-SNHG1 can greatly attenuate cell viability and S cell ratio (P < 0.05), and increase G0/G1 cell ratio, apoptosis rate, Cleaved Caspase-3, CHOP, and ATF4 protein level (P < 0.05) compared to the si-NC group. Furthermore, the double luciferase reporter experiment confirmed that SNHG1 can competitively combine withmiRNA-100-3p. Also, co-transfection of si-SNHG1 and anti-miRNA-100-3p could significantly increase cell viability and S cell ratio (P < 0.05), and decrease G0/G1 cell ratio and apoptosis rate, and Cleaved Caspase-3, CHOP, and ATF4 protein levels compared to si-SNHG1+anti-miRNA-NC (P < 0.05). Interfering with SNHG1 could inhibit the proliferation of Ishikawa cells and promote apoptosis by upregulating miRNA-100-3p expression.

2Fibulin-5 Inhibits Proliferation of Endometrial Carcinoma Ishikawa Cells by Down-Regulating β-Catenin

2020 ◽  
Vol 10 (2) ◽  
pp. 189-194
Author(s):  
Jing Chu ◽  
Zhichao Tong ◽  
Xiaolan Zhou ◽  
Teng Li
Keyword(s):  
Endometrial Cancer ◽  
Cell Viability ◽  
Endometrial Carcinoma ◽  
Cancer Cell Proliferation ◽  
Ishikawa Cells ◽  
Cancer Tissues ◽  
Related Pathway ◽  
Tissue Cancer

Endometrial cancer is a malignance in the uterus. The incidence of endometrial cancer is increasing recent years. Fibulin-5 participates in tissue homeostasis. The exact role of Fibulin-5 in endometrial cancer, such as becoming a sensitive tumor marker for endometrial cancer for diagnosis and follow-up, remains to be determined. 30 cases of endometrial tissue cancer specimens and adjacent tissues were collected for analysis of the expression of Fibulin-5 by western blot. Endometrial carcinoma Ishikawa cells (ECICs) were cultured and the level of Fibulin-5 was regulated via transfection. β-catenin level was measured followed by analysis of cell viability by MTT assay or BrdU staining. Results showed that Fibulin-5 in endometrial carcinoma tissues was significantly downregulated compared to para cancer tissues. Overexpression of Fibulin-5 decreased cell viability of endometrial carcinoma Ishikawa cells (ECICs) whereas downregulation increased cell viability. Meanwhile, Fibulin-5 overexpression significantly downregulated β-catenin and β-catenin knockdown blocked the proliferation effect caused by Fibulin-5 on ECICs. In conclusion, Fibulin-5 could inhibit cancer cell proliferation possibly via β-catenin related pathway.

Long non-coding RNA Linc00525 as a prognostic factor to regulate proliferation and apoptosis in colorectal cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15085-e15085 ◽  
Author(s):  
Peng Peng ◽  
Qin Zheng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Qrt Pcr ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

e15085 Background: Colorectal cancer (CRC) is one of the most common digestive system tumors and poses a serious threat to human health. More and more studies have shown that long noncoding RNAs (lncRNAs) play an important role in the occurrence and development of various tumors. They regulate a variety of cancer biology, such as proliferation, apoptosis, invasion and metastasis. Abnormally expressed lncRNAs are closely related to colorectal cancer. The purpose of this study was to find lncRNAs associated with the development of colorectal cancer and to explore its function and mechanism. Methods: (1) By analyzing the expression profile of lncRNAs in colorectal cancer-normal tissues in GEO databases, the abnormal expression of lncRNA LINC00525 was screened. Colorectal cancer tissues, adjacent normal colon tissues and colorectal cancer cell lines (HCT116, DLD1, HT-29, SW480) were detected by qRT-PCR. We analyzed the relationship between expression of LINC00525 and clinical features. (2) The biological functions of LINC00525 in HCT116, DLD1 and SW480 were peformed in vitro by MTT, clone formation assay, EDU and flow cytometry. (3) The effect of LINC00525 on tumorigenesis in vivo was evaluated by nude mice model. (4) The expression of lncRNA LINC00525 was knocked down in colorectal cancer cell lines (HCT116, SW480), and the mRNA expression levels of P15, P21, P27 and KLF2 were detected by qRT-PCR. Results: (1) Microarray data and qRT-PCR verification showed that the expression of lncRNA LINC00525 in colorectal cancer tissues and colorectal cancer cell lines was significantly upregulated. The overexpression of LINC00525 was positively correlated with clinical stage and tumor size. (2) Knockdown of LINC00525 in colorectal cancer cell lines could inhibit cancer cell proliferation and induce apoptosis. In SW480 and HCT116 cell lines, cells were arrested in G0/G1 phase after knocking down LINC00525. (3) Subcutaneous xenograft experiments in nude mice further confirmed that knockdown of LINC00525 could inhibit the tumor growth. (4) After knocking down the expression of LINC00525 in HCT116 and SW480 cell lines, the expression of mRNAs of tumor suppressor genes P15, P21, P27 and KLF2 increased. Conclusions: Our studies suggested that LINC00525 was significantly upregulated in colorectal cancer tissues. Mechanism studies had shown that LINC00525 could regulate the expression of KLF2, P15, P21 and P27 in CRC cell lines, and then affect cell proliferation and apoptosis.

Molecular Mechanism of circRAPGEF5 in Regulating the Molecular Axis of microRNA-4712-5p/Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Epsilon Affecting Cellular Proliferation and Apoptosis in Mammary Cancer

2021 ◽  
Vol 11 (6) ◽  
pp. 1053-1058
Author(s):  
Tao Chen ◽  
Shengrong Sun
Keyword(s):  
Western Blot ◽  
Cancer Cells ◽  
Mammary Cancer ◽  
Caspase 3 ◽  
Cellular Proliferation ◽  
Molecular Axis ◽  
Luciferase Reporter ◽  
Qrt Pcr ◽  
Proliferation And Apoptosis ◽  
Reporter Assays

To understand the molecular mechanism of circRAPGEF5, its effect on the proliferation and apoptosis of mammary cancer cells, and its regulatory effect on the molecular axis of miRNA-4712-5p/YWHAE. qRT-PCR and Western blot were used to test circRAPGEF5, miRNA-4712-5p, and YWHAE expression in mammary cancer and paracancerous tissues. The human mammary cancer cell, MDA-MB-231, was cultured in vitro, and pcDNA-NC, pcDNA-circRAPGEF5, anti-miRNA-NC, anti-miRNA-4712-5p, pcDNA-circRAPGEF5, and miRNA-NC, pcDNA-circRAPGEF5 were transfected into MDA-MB-231 cells with miRNA-4712-5p mimics. qRT-PCR and Western blot were employed to detect circRAPGEF5, miRNA-4712-5p, and YWHAE expression in cells. The CCK-8 methodand plate clone formation experiment were conducted to test cellular proliferation ability. Flow cytometry was performed to detect apoptosis rate. Dual luciferase reporter assays were used to test the targeting association between circRAPGEF5 and miRNA-4712-5p, and the targeting association between miRNA-4712-5p and YWHAE. Western blot was utilized to detect Bcl-2, Bax, and Cleared Caspase-3 protein expression. In comparison with paracancerous tissues, circRAPGEF5 and YWHAE expression levels in mammary cancer tissues were significantly reduced (P < 0.05), and miRNA-4712-5p expression levels were significantly increased (P < 0.05). Transfection of pcDNA-circRAPGEF5 or trans-anti-miRNA-4712-5p could reduce the optical density (OD) value, Bcl-2 protein level and clonal formation number to a significant extent (P < 0.05), and it increases Bax and Cleaved Caspase-3 apoptosis rate and protein levels (P < 0.05). Dual luciferase reporter assays confirmed that there was target binding between circRAPGEF5 and miRNA-4712-5p and between miRNA-4712-5p and YWHAE. Co-transfection of pcDNA-circRAP GEF5 and miRNA-4712-5p could greatly reduce transfection of pcDNA-circRAP GEF5 and its effect on the proliferation and apoptosis of MDA-MB-231 cells. Overexpression of circRAPGEF5 can inhibit the proliferation of mammary cancer cells and induce apoptosis by regulating the molecular axis of miRNA-4712-5p/YWHAE.

scholarly journals Medroxyprogesterone acetate causes the alterations of endoplasmic reticulum related mRNAs and lncRNAs in endometrial cancer cells

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenjiao Cao ◽  
Wuyuan Gao ◽  
Panchan Zheng ◽  
Xiao Sun ◽  
Lihua Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Endometrial Cancer ◽  
Er Stress ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Inhibitory Effect ◽  
Functional Enrichment ◽  
Qrt Pcr ◽  
Ishikawa Cells ◽  
Ec Cells

Abstract Background Progestin is effective to promote endometrial cancer (EC) cells apoptosis, however, continuous progestin administration causes low level of progestin receptor B (PRB), further resulting in progestin resistance. Here, we performed microarray analysis on Ishikawa cells (PRB+) treated with medroxyprogesterone acetate (MPA) to explore the molecular mechanism underlying the inhibitory influence of MPA on PRB+ EC cells. Methods Microarray analysis was performed by using Ishikawa cells (PRB+) treated with MPA. Differentially expressed mRNA and long noncoding RNAs (lncRNAs) were identified. Furthermore, the functions of these mRNAs and lncRNAs were predicted by functional enrichment analysis. QRT-PCR was further performed to verify the microarray data. Results A total of 358 differentially expressed genes and 292 lncRNAs were identified in Ishikawa cells (PRB+) treated with MPA. QRT-PCR verified these data. Functional enrichment analysis identified endoplasmic reticulum (ER) stress as the key pathway involved in the inhibitory effect of MPA on EC cells. And the ER stress apoptotic molecule CHOP and ER stress related molecule HERPUD1 were both highly expressed in Ishikawa cells (PRB+) treated with MPA. Co-expression analysis showed lnc-CETP-3 was highly correlated with CHOP and HERPUD1, suggesting it might participate in ER stress pathway-related EC cell apoptosis caused by MPA. In addition, compared with untreated cells, lnc-CETP-3, CHOP and HERPUD1 were significantly up-regulated in Ishikawa cells (PRB+) treated with MPA, whereas they have no statistical significance in KLE cells (PRB-). Conclusions MPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+. Lnc-CETP-3 might be involved in this process. These findings may provide therapeutic targets for EC patients with PRB-, and resistance-related targets to increase the sensitivity of MPA on EC cells.

scholarly journals Hydroethanolic Extracts of the Aristotelia Chilensis (Maqui) Berry Reduces Cellular Viability and Invasiveness in the Endometrial Cancer Cell Line Ishikawa

2021 ◽  
Vol 20 ◽  
pp. 153473542110075
Author(s):  
Javier Mena ◽  
Estefanía Elgueta ◽  
Francisca Espinola-Gonzales ◽  
Hugo Cardenas ◽  
Pedro A. Orihuela
Keyword(s):  
Endometrial Cancer ◽  
Cell Viability ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Boyden Chamber ◽  
Female Population ◽  
Endometrial Cancer Cell ◽  
Ishikawa Cells ◽  
Aristotelia Chilensis

Cancer of the reproductive tract includes diseases with higher prevalence in the female population. This investigation examined whether an anthocyanin-enriched extract of Aristotelia chilensis, commonly known as “maqui,” could affect some hallmarks of endometrial cancer. Cultures of the human endometrial cancer cell line Ishikawa were treated with a hydroethanolic maqui extract at 1, 3, 10, 30, 100, 300, or 1000 µg/mL to determine the effect on cell viability by MTT assay. Then, we used the 50% Effective Concentration (EC50) to evaluate whether the effect of the maqui extract is mediated via an arrest of the cell cycle or induction of apoptosis using flow cytometry or Annexin V-FITC assays, respectively. The effects of sublethal doses of the maqui extract on migration and invasiveness of Ishikawa cells were also evaluated by the wound healing and Boyden Chamber assay, respectively. Our results show that the hydroethanolic maqui extract inhibits the cell viability with an EC50 of 472.3 µg/mL via increased apoptosis, and that reduces the invasive capacity but not migration of Ishikawa cells. These findings suggest that the hydroethanolic maqui extract has antineoplastic properties for endometrial cancer and merits further studies to corroborate its efficiency as anticancer therapy in reproductive organs.

scholarly journals Serum amyloid a, a potential biomarker both in serum and tissue, correlates with ovarian cancer progression

2019 ◽  
Author(s):  
Ze Li ◽  
Yongwang Hou ◽  
Meng Zhao ◽  
Tianning Li ◽  
YaHui Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Migration ◽  
Akt Pathway ◽  
Pcr Assay ◽  
Amyloid A ◽  
Qrt Pcr ◽  
Pathway Activation ◽  
Treatment Prediction ◽  
Potential Biomarker ◽  
Cancer Tissues

Abstract Objective: Ovarian cancer is the most fatal gynecologic malignancy worldwide due to delayed diagnosis as well as recurrence and drug resistance. Thus, a new type of ovarian cancer treatment prediction biomarker is urgently needed to supplement existing tools. Methods: One hundred patients operated on due to ovarian tumor were enrolled in this study. Meanwhile, one hundred ovarian benign patients and thirty healthy women were selected as control groups. Levels of SAA, CA125 and HE4 were assessed using standard laboratory protocols. 5 ovarian cancer tissues and paracancerous tissues were collected and than stored at -80℃ until the qRT-PCR assay was conducted.Results: The ROC curve of SAA concentration in ovarian cancer was plotted to obtain the area under the curve AUC = 0.889, the cut-off value 17.05 mg/L, the sensitivity 78.4% and specificity 86.5%. The results by logistic regression analysis revealed that there was significant correlation between the level of serum SAA and clinical stage and lymph node and distant metastasis. Compared with pre-treatment, the level of serum SAA decreased significantly after treatment. qRT-PCR assay revealed that the mRNA of SAA-1 and SAA-4 was much higher in cancer tissues than in adjacent tissues, and MMPs was up-regulation including MMP-1, MMP-9 and MMP- 12 in OVCAR-3 cell stimulated by SAA and transwell assay revealed that SAA could promote OVCAR-3 cell migration. Moreover, SAA can regulate EMT markers and promote Akt pathway activation.Conclusion: In summary, our results demonstrated that SAA may be a potential diagnosis and treatment prediction biomarker. SAA promote OVCAR-3 cell migration by regulating MMPs and EMT which may correlate with Akt pathway activation.

scholarly journals MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

2020 ◽  
Author(s):  
Suxian Lin ◽  
Zhiyong Zhang ◽  
Shengnan Wang ◽  
Yang Lu ◽  
Meilv Yang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Protein Expression ◽  
Caspase 3 ◽  
Healthy Controls ◽  
Quantitative Real Time Pcr ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Synovial Tissues ◽  
Fibroblast Like Synoviocytes

Abstract Background: Growing data have indicated that fibroblast-like synoviocytes (FLS) and miRNAs are implicated in the pathogenesis of rheumatoid arthritis (RA). This study was aimed to evaluate the function of miR-6089 in the regulation of RA-FLSs. Methods: The expression of miR-6089 was measured by quantitative real time PCR (qRT-PCR). The RA-FLSs were transfected with si-CCR4 plasmids or miR-6089 mimic, and subjected to CCK-8 and flow cytometry to analyze proliferation and apoptosis. The concentrations of MMP-1, TNF-α and IL-6 in RA-FLSs supernatant were detected using ELISA. The protein expression of caspase-3, -8 and -9 was detected using western blot.Results: The levels of miR-6089 were detected to be significantly lower in the synovial tissues and FLSs of RA than in the synovial tissues and FLSs of healthy controls. The miR-6089 up-regulation in RA-FLSs significantly inhibited the proliferation and promoted cell apoptosis accompany with an increase protein expression of caspase-3, -8 and -9. Furthermore, CCR4 was determined to directly target miR-6089, and its expression was significantly increased in the synovial tissues of RA than in the synovial tissues of healthy controls. Moreover, CCR4 overexpression effectively reversed the effect on proliferation and apoptosis induced by miR-6089 in RA-FLSs. Conclusion: Our results revealed that miR-6089 may be a potential target for RA prevention and therapy of RA.

Effects of LncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Regulating Bcl-2 on Glioma Cell Proliferation and Apoptosis Through Regulating MiR-204 Expression

2020 ◽  
Vol 10 (2) ◽  
pp. 234-238
Author(s):  
Zheng Lin ◽  
Hui Wang ◽  
Junyou Wang ◽  
Gaojun Lin ◽  
Da Lin
Keyword(s):  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Line ◽  
Cell Apoptosis ◽  
Glioma Cell ◽  
Rna Expression ◽  
Qrt Pcr ◽  
Lncrna Malat1 ◽  
Proliferation And Apoptosis ◽  
Glioma Cell Proliferation

Objective: To investigate lncRNA MALAT1’s effect on glioma cell proliferation and apoptosis. Methods: qRT-PCR was applied to detect the MALAT1 RNA expression in para-carcinoma and carcinoma tissues of patients with brain glioma. After MALAT1 knockdown with small interfering RNA (siRNA) in U87 cell line, MALAT1 and miR-204 expression levels were measured by qRT-PCR and cell proliferation was measured by CCK-8 assay. The U87 cell line with overexpressed miR-204 expression was constructed and miR-204 expression was detected by qRT-PCR. The CCK-8 assay and flow cytometer were adopted to determine cell proliferation and apoptosis, respectively. Annexin V/propidium iodide (AV/PI) staining was conducted to detect cell apoptosis. Targets can target gene prediction website predicted the target of miR-204 and Bcl-2 level was detected by qRT-PCR and Western blot. Results: MALAT1 RNA in glioma tissues was significantly upregulated compared to para-carcinoma tissues (p < 0.05). After MALAT1 RNA expression was down-regulated by trans-fecting of MALAT1 siRNA, miR-204 expression was elevated, while cell viability was reduced. Moreover, overexpression of miR-204 significantly decreased Bcl-2 mRNA and protein level (p < 0.05), reduced cell viability (p < 0.05), and increased cell apoptosis rate (p < 0.05). Conclusion: miR-204 can be up-regulated by suppressing lncRNA MALAT1 expression, thus controlling Bcl-2 expression, resulting in inhibition of proliferation of glioma cells and promotion of cell apoptosis.

scholarly journals Vascular Endothelial Growth Factor Ameliorated Palmitate Induced Cardiomyocyte Injury via JNK Pathway

2020 ◽  
Author(s):  
Shiya Wang ◽  
Cao Zou ◽  
Xiaofeng Liu ◽  
Yonjin Yan ◽  
Shunzhon Gu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Western Blot ◽  
Cell Viability ◽  
Mtt Assay ◽  
Caspase 3 ◽  
Time Dependent ◽  
Control Group ◽  
Apoptosis Rate ◽  
Dependent Relation ◽  
Quantitative Fluorescence

Abstract Objective To investigate the effect of palmitate (PAL) on apoptosis and the timing and activity of VEGF expression in HHHM2 myocardial cells (a human embryonic cardiomyocyte cell- line). Methods 1. Cardiomyocytes were divided into the following five groups: the control group and the 0.2 mM, 0.5 mM, 0.8 mM, and 1.2 mM PAL groups. We examined the changes in cell viability by MTT assay after PAL incubation for 24 h and the cardiomyocyte apoptosis rate by FACS examination, and thus determined the effective concentration of PAL. The transcription levels of CASP3, Bcl-2, Bax, and VEGF were detected by quantitative fluorescence PCR and the protein expression of caspase 3 and VEGF by western blot. 2. To observe the time-dependent effects on cell injury induced by 0.5 mM PAL, cardiomyocytes were divided into 0, 4, 8, 16, 24, and 48 h groups. The variation in cell viability was examined by MTT assay. The transcription levels of CASP3, Bcl-2, Bax, and VEGF were detected by quantitative fluorescence PCR and the protein expression of caspase 3 and VEGF by western blot. 3. To observe the effects of VEGF on the PAL induced apoptosis of cardiomyocytes, the cells were divided into the control group and the VEGF overexpression group. At 24 h after transfection, cells were incubated with 0.5 mM PAL for 6, 12, 24, and 48 h. Cell viability was examined by MTT assay. The apoptosis rate was measured by FACS using the Annexin V-FITC kit. The transcription levels of CASP3, Bcl-2, Bax, NF-kB p65, and VEGF were measured by quantitative fluorescence PCR, the protein expression of VEGF, caspase 3, Bcl-2, Bax, NF-κB p65, p-JNK/JNK, and p-ERK/ERK were measured by western blot, as well as caspase 3 activity. Results 1. A dose-dependent relation between the concentration of PAL and H9c2 cardiomyocyte injury was observed. In the 0.5 mM group, the apoptosis rate was increased significantly, while cell viability was decreased, indicating that 0.5 mM PAL was the ideal concentration to induce cardiomyocyte apoptosis. The expression of caspase 3 and Bax was significantly increased, and the expression of VEGF was enhanced, while the levels of Bcl-2 remained unchanged during the process. 2. A significant time-dependent relation between PAL and cardiomyocyte injury was observed. The apoptosis rate was increased greatly after 16 h treatment with 0.5 mM PAL. 3. Cell viability was restored by VEGF overexpression during treatment with 0.5 mM PAL. The apoptosis rate was also reduced by VEGF overexpression, as detected by FACS. The expression of caspase 3, Bax, and NF-κB p65 was significantly decreased, Bcl-2 and VEGF expression was dramatically increased, p-JNK/JNK expression was significantly enhanced, p-ERK/ERK levels did not exhibit a significant change, and the activity of caspase 3 was significantly decreased. Conclusions 1. PAL can induce injury and apoptosis in HHHM2 myocardial cells, and these effects are time-dependent. A PAL concentration of 0.5 mM was ideal to establish the cardiac cell injury model. 2. PAL at a concentration of 0.5 mM can effectively induce cardiomyocyte injury and enhance the expression of caspase 3, Bax, and VEGF, especially after 24 h and 48 h of PAL treatment. 3. VEGF overexpression can reverse the effects of PAL on apoptosis and cell viability. In addition, VEGF overexpression inhibited the expression of proapoptotic and inflammatory factors, caspase 3 activity, and transduction of the MAPK signaling pathway.

scholarly journals The Inhibition of Long Non-Coding RNA CAR10 and The Regulation of miR-203 Expression Suppresses Cell Viability and Induces Cell Apoptosis in Prostate Cancer

2020 ◽  
Author(s):  
Liansheng Zhang ◽  
Yougan Chen ◽  
Zhenjie Wang ◽  
Qiang Xia
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Gene Assay ◽  
Long Non Coding Rna

Abstract Background: Prostate cancer (PC) is one of the most common malignant tumors. Recently, it has been reported that long noncoding RNAs (lncRNAs) play key roles in tumor progression. Studies have revealed that long non-coding RNA CAR10 (CAR10) can regulate tumor cell behaviors through sponging miR-203. In this study, we examined the effects of CAR10 in PC cells. Methods: Firstly, real time-quantitative polymerase chain reaction (qRT-PCR) was used to explore CAR10 expression in tumor tissues, peripheral blood of PC patients, and PC cells. We used the dual-luciferase reporter gene assay to analyze the relationship between CAR10 and miR-203. Moreover, flow cytometry, MTT assay, and western blot assay were used to determine cell apoptosis, cell viability, and apoptosis-related protein expression. Results: The results showed that CAR10 expression was remarkably higher in PC samples compared with that of control, and CAR10 regulated miR-203 negatively in PC cells. The qRT-PCR results also showed that miR-203 expression was significantly decreased in PC samples. Moreover, knockdown of CAR10 inhibited PC cell viability and promoted cleaved caspase-3 expression but induced PC cell apoptosis and, reduced pro-caspase-3 expression; miR-203 inhibitor reversed these effects. Conclusion: Our study found that CAR10 is a potential oncogene in PC and suggests that CAR10 inhibition could inhibit PC cell viability but promote PC cell apoptosis through regulating miR-203 expression. Our results show that CAR10 is a potential target for the treatment of PC.

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