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HMGA1P4 is upregulated in DDP-resistant GC tissues and cells, and triggers the progression of DDP-resistance in GC.
We aimed at observing the correlation between microRNA-766 expression and the efficacy of platinum-containing chemotherapy in patients with stage IV gastric cancer (GCa).
Tissue specimens were obtained from 100 patients with stage IV GCa who received platinum-based chemotherapy, and microRNA-766 expression in these samples was examined by quantitative real-time polymerase chain reaction (qPCR) analysis. Survival analysis was carried out through Kaplan-Meier test. The influencing factors of survival were assessed through COX univariate and multivariate regression.
GCa tissues contained significant lower expression of microRNA-766 than adjacent tissues. The degree of tumor differentiation and peritoneal metastasis were confirmed to have great relevance to microRNA-766 level. Patients with high microRNA-766 expression have better chemotherapy efficacy and longer progression-free survival.
Our study shows for the first time that the highly expressed microRNA-766 in tumor tissues of patients with stage Ⅳ GCa predicts better platinum-containing chemotherapy efficacy and prognosis.
Our study shows for the first time that the highly expressed microRNA-766 in tumor tissues of patients with stage Ⅳ GCa predicts better platinum-containing chemotherapy efficacy and prognosis.
Colorectal cancer (CRC) has a very high morbidity and mortality worldwide. Related studies have shown that microRNA-543 (miR-543) is involved in the development of many cancers, including CRC. The purpose of this study was to explore the potential molecular mechanism of miR-543's involvement in the development of CRC.
QRT-PCR and Western blot were used to detect the expression of proliferation and migration-related proteins, signal transduction and transcriptional activator 3 and protein inhibitor of activated signal transducer and activators of transcription 3 (PIAS3). Cell proliferation and metastasis were measured by MTT, transwell and Western blot. The binding sites of miR-543 and PIAS3 were predicted by TargetScan database and verified by double-luciferase report experiment.
The expression of miR-543 was high in CRC tissues and cell lines, while the mRNA and protein levels of PIAS3 were decreased. Meanwhile, a negative correlation between miR-543 and PIAS3 was also observed in CRC tissues. Moreover, the downregulation of miR-543 led to the inhibition of viability and the expression of proliferation and migration related proteins. Subsequently, miR-543 depletion also blocked cell migration and invasion. MiR-543 inhibits the expression of PISA3. Furthermore, downregulation of PIAS3 undermined the miR-543 depletion-mediated suppression effect on SW480 and LOVO cells. Notably, loss of miR-543 downregulated STAT3 activity, which was rescued by PIAS3 ablation.
MiR-543 participated in cell proliferation and metastasis by targeting PIAS3 in CRC.
MiR-543 participated in cell proliferation and metastasis by targeting PIAS3 in CRC.
Pancreatic cancer is a gastrointestinal tumor with the highest malignancy and few diagnostic and prognostic markers. Patients with disease have a 5-year survival rate that is not more than 10%. As a research hotspot in recent years, miRs (microRNAs) are differentially expressed in various tumors, so they can be used as the potential diagnostic and prognostic markers. In this study, differentially expressed miRs in patients with pancreatic cancer were screened out through the GEO chip, to provide potential markers for clinical practice. This study aimed to explore the expression and potential value of miR-4730 in pancreatic cancer.
Differentially expressed miRs in pancreatic cancer were analyzed through logging in GEO DataSets to download GSE112264. Fifty patients with pancreatic cancer who were treated in our hospital from May 2012 to January 2014 (Group A), 50 patients with benign pancreatic lesions during the same period (Group B), and 50 healthy individuals undergoing physical examinations (Group C) we stages III+IV of pancreatic cancer had higher incidences of lymphatic invasion and distal metastasis (p<0.05), so miR-4730 had a diagnostic value. The 3- and 5-year survival rates in the high miR-4730 expression group were higher than those in the low expression group (both p<0.05). TNM staging, lymphatic invasion, distal metastasis, and miR-4730 were independent prognostic factors for the 3- and 5-year survival of patients with pancreatic cancer.
For patients with pancreatic cancer, those with low miR-4730 expression have poor survival and prognoses, so miR-4730 can be used as a potential observational index for the prognosis and diagnosis of the disease.
For patients with pancreatic cancer, those with low miR-4730 expression have poor survival and prognoses, so miR-4730 can be used as a potential observational index for the prognosis and diagnosis of the disease.
Accumulating evidence verified that microRNAs (miRNAs) participate in the development of several cancers.
The levels of miR-138-5p and forkhead box c1 (FOXC1) were examined using quantitative Real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8), colony formation, migration, and Transwell invasion assays were conducted to examine the impact of miR-138-5p on hepatocellular carcinoma (HCC) cells. The protein expression of FOXC1 was detected using Western blotting assay. The tumor growth of HCC cell in vivo was analyzed using transplanted tumor model. The expressions of FOXC1 and Ki67 in vivo were assessed using immunohistochemistry (IHC) assay.
We testified that miR-138-5p was down-expressed in HCC and the low level of miR-138-5p was related to the poor clinical outcome of patient with HCC. Moreover, miR-138-5p repressed the growth and metastatic phenotypes of HCC cells. Consistent with the results in vitro investigations, we revealed that miR-138-5p served as a suppressive miRNA in the growth of HCC cell in vivo. By using the luciferase assay and immunoblotting, we validated that FOXC1 was a potential downstream gene of miR-138-5p. Finally, our results showed that re-expression of FOXC1 rescued the growth and metastatic-related traits of HCC cell inhibited by miR-138-5p.
Altogether, our observations imply that miR-138-5p restrains the aggressive phenotypes of HCC cell via modulating FOXC1.
Altogether, our observations imply that miR-138-5p restrains the aggressive phenotypes of HCC cell via modulating FOXC1.
LncRNA differentiation antagonizing non-protein coding RNA (DANCR) is an oncogene in various malignant cancers, including hepatocellular carcinoma (HCC). Autophagy is an intracellular self-digestion mechanism that accelerates the progression of HCC via promoting cell survival. However, the role of lncRNA DANCR in HCC, and the mechanism of lncRNA DANCR in the regulation of autophagy in HCC remains unknown. Therefore, the aims of this study are the investigation of the role of lncRNA DANCR in HCC, and the exploration of the molecular mechanism of lncRNA DANCR in regulating autophagy of HCC cells.
In this study, the expression of lncRNA DANCR, miR-222-3p, and autophagy-related gene 7 (ATG7) was detected by qRT-PCR. The cell proliferation and colony formation were measured by Cell Counting Kit-8 (CCK-8) assay and colony formation assay. And the autophagic flux was evaluated by mRFP-GFP-LC3B reporter. The autophagy related proteins were analyzed by Western blotting. Besides, the relationship between lncRNA DANCR and miR-222-3p, as well as between miR-222-3p and ATG7, was determined by Dual-Luciferase reporter system.
We found high expression of lncRNA DANCR and ATG7, and low expression of miR-222-3p in HCC tissues and cell lines. And lncRNA DANCR positively correlated with poor survival of HCC patients. Moreover, the knockdown of lncRNA DANCR inhibited cell proliferation and autophagy of HCC cells. And we predicted and proved that lncRNA DANCR induced cell proliferation, colony formation and autophagy by increasing ATG7 and suppressing miR-222-3p.
Our study demonstrates the promoting role of lncRNA DANCR in HCC, and indicates the regulatory effects of lncRNA DANCR on regulating autophagy of HCC.
Our study demonstrates the promoting role of lncRNA DANCR in HCC, and indicates the regulatory effects of lncRNA DANCR on regulating autophagy of HCC.
Liver cancer is the second most common cause of cancer death, causing more than 700,000 deaths every year. It has been demonstrated that Long non-coding RNA (LncRNA) plays an important regulatory role in a series of diseases. However, the regulatory mechanism of LncRNAs in liver cancer has not been fully elucidated. The purpose of this study was to explore the interaction of lncRNA HOTAIRM1 and aberrant histone modification in liver cancer.
qRT-PCR was used to detect the expression levels of RIZ1 and miR-125b in liver cancer cells. Cell proliferation was measured using the CCK8 assay. ChIP-Real-time PCR confirmed the binding site of the promoter of HOTAIRM1 by H3K9me1. The direct target of HOTAIRM1 and miR-125b in liver cancer cells was measured by a luciferase reporter assay. this website Cell proliferation was detected by Cell Counting Kit-8 (CCK8). Cell invasion was measured by transwell assays and cell migration was detected by wound healing assay.
The expression level of RIZ1 and miR-125b was upregulated, and H liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. It may serve as a therapeutic marker for liver cancer treatment.
For the first time, we found that RIZ1 was upregulated in liver cancer cells and RIZ1-mediated H3K9me1 enrichment on the HOTAIRM1 promoter regulated the growth and metastasis of liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. It may serve as a therapeutic marker for liver cancer treatment.
Amongst noncoding RNAs, competing endogenous RNAs (ceRNAs) are popular and interesting regulatory mechanisms involved in oncogenesis and tumour progression. LncRNA FGD5-AS1, also known as miR-5590-3p, is involved in the regulatory role of ceRNA in many cancers. However, the roles of lncRNA FGD5-AS1 or miR-5590-3p in renal cell carcinoma (RCC) remain unclear. We investigated how FGD5-AS1 and miR-5590-3p regulated clear cell proliferation and metastasis in RCC.
Real Time-quantitative PCR (RT-qPCR) was used to detect the expression of FGD5-AS1 in tumour issues and renal cancer cell lines. MTT, scratch test and transwell assay were performed to confirm the effect of FGD5-AS1 on the proliferation, migration or invasion of the above cell lines. RNA pull-down and Luciferase assays were used to detect the target site between FGD5-AS1 and miR-5590-3p. In addition, we examined the proteins related to ERK/AKT signalling related via Western blot analysis. Finally, we used the RT-qPCR method to detect the mRNA levels malignancy of tumours. This lncRNA could become a potential target molecule for treating and diagnosing RCC.
It was the aim of this study to explore the role and mechanism of long non-coding RNA (lncRNA) AFAP1-AS1 in the progression of bladder cancer (BCa) by in vitro experiments.
AFAP1-AS1 levels in 40 pairs of clinical BCa tissue samples and normal ones collected from BCa patients were determined, and paired sample t-test was applied to compare the differences between groups. The prognosis data of patients with BCa were collected, and survival analysis and t-test were performed to specify the interplay between AFAP1-AS1 and the prognosis of BCa patients. Subsequently, AFAP1-AS1 expression level in BCa and normal cells were further confirmed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU), and transwell assays were performed to figure out the influence of this lncRNA on the proliferation ability and invasiveness of BCa cells. Meanwhile, the interaction between AFAP1-AS1 and its sense mRNA was analyzed. We used co-transfection technology to simultaneously transfect si-AFAP1-AS1 and pcDNA3.
