scholarly journals Long non-coding RNA Lnc-LALC facilitates colorectal cancer liver metastasis via epigenetically silencing LZTS1

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Chuan Zhang ◽  
Lu Wang ◽  
Chi Jin ◽  
Jiahui Zhou ◽  
Chaofan Peng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Liver Metastasis ◽  
Malignant Tumors ◽  
Methylation Status ◽  
Dna Methyltransferases ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractColorectal cancer (CRC) is one of the most common cancers around the world and endangers human health seriously. Liver metastasis is an important factor affecting the long-term prognosis of CRC and the specific mechanism of CRLM (colorectal cancer with liver metastasis) is not fully understood. LZTS1 has been found dysregulated in many cancers, especially in CRC. Theories suggested that hypermethylation of the promoter regions of LZTS1 was responsible for LZTS1 abnormal expression in multiple malignant tumors. Although the role of LZTS1 in CRC cell proliferation has been reported, its role in CRLM remains unclear. Numerous studies reported Long non-coding RNA (lncRNA) could regulate the gene expression level by regulating gene methylation status in many tumors. However, whether there were lncRNAs could change the methylation status of LZTS1 or not in CRLM was unknown. In this study, we aimed to investigate whether there are lncRNAs can regulate the expression of LZTS1 through affecting DNA methylation in CRLM. We found that upregulated Lnc-LALC in CRC was negatively correlated with LZTS1 expression, and Lnc-LALC could regulate LZTS1 expression in both mRNA and protein level in our study. Functionally, Lnc-LALC enhanced the CRC cells metastasis ability in vitro and vivo through inhibiting the expression of LZTS1. Furthermore, the precise mechanisms exploration showed that lnc-LALC could recruit DNA methyltransferases (DNMTs) to the LZTS1 promoter by combining with Enhancer of zeste homolog 2(EZH2) and then altered the expression of LZTS1 via DNMTs-mediated DNA methylation. Collectively, our data demonstrated the important role of Lnc-LALC/ LZTS1 axis in CRLM development.

The role of long non-coding RNA AFAP1-AS1 in human malignant tumors

2018 ◽  
Vol 214 (10) ◽  
pp. 1524-1531 ◽  
Author(s):  
Daolin Ji ◽  
Xiangyu Zhong ◽  
Xingming Jiang ◽  
Kaiming Leng ◽  
Yi Xu ◽  
...  
Keyword(s):  
Malignant Tumors ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Human Malignant Tumors

The Role of Tumor-related LncRNA PART1 in cancer

2021 ◽  
Vol 27 ◽  
Author(s):  
Jinlan Chen ◽  
Enqing Meng ◽  
Yexiang Lin ◽  
Yujie Shen ◽  
Chengyu Hu ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
Toll Like Receptor ◽  
Non Coding Rna ◽  
Regulated Expression ◽  
The One ◽  
Long Non Coding Rna

Background: As we all know, long non-coding RNA (lncRNA) affects tumor progression, which has caused a great upsurge in recent years. It can also affect the growth, migration, and invasion of tumors. When we refer to the abnormal expression of lncRNA, we will find it associated with malignant tumors. In addition, lncRNA has been proved to be a key targeted gene for the treatment of some diseases. PART1, a member of lncRNA, has been reported as a regulator in the process of tumor occurrence and development. This study aims to reveal the biological functions, specific mechanisms, and clinical significance of PART1 in various tumor cells. Methods: Through the careful search of PUBMED, the mechanisms of the effect of PART1 on tumorigenesis and development are summarized. Results: On the one hand, the up-regulated expression of PART1 plays a tumor-promoting role in tumors, including lung cancer, prostate cancer, bladder cancer and so on. On the other hand, PART1 is down-regulated in gastric cancer, glioma and other tumors to play a tumor inhibitory role. In addition, PART1 regulates tumor growth mainly by targeting microRNA such as miR-635, directly regulating the expression of proteins such as FUS/EZH2, affecting signal pathways such as the Toll-like receptor pathway, or regulating immune cells. Conclusion: PART1 is closely related to tumors by regulating a variety of molecular mechanisms. In addition, PART1 can be used as a clinical marker for the early diagnosis of tumors and plays an important role in tumor-targeted therapy.

scholarly journals Long non-coding RNA THOR promotes Ovarian Cancer cells progression via STAT3 pathway

2020 ◽  
Author(s):  
Jing Ge ◽  
Tao Han ◽  
Lili Shan ◽  
Jing Na ◽  
Ya Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Malignant Tumors ◽  
Ovarian Cancer Cells ◽  
Self Renewal ◽  
Stat3 Signaling ◽  
Non Coding Rna ◽  
The Impact ◽  
Long Non Coding Rna

Abstract Background Ovarian cancer (OC) is one of the most common malignant tumors in the world. The prognosis of OC remains poor due to the advanced stage and distant metastasis at the time of diagnosis. Recently, a novel lncRNA, THOR (testis-associated highly conserved oncogenic long non-coding RNA), was characterized in human cancers and shown to exhibit an oncogenic role. However, the role of THOR in OC was still unknown.Methods RT-PCR and western blot analysis were used to detect the expression of THOR and p-STAT3. The impact of THOR on OC proliferation, metastasis and self-renew was investigated in vitro and in vivo . The prognostic value of THOR was determined in OC patient cohorts.Results In this study, our results found that THOR was markedly upregulated in human OC tissues and predict the poor prognosis of OC patients. THOR knockdown resulted in significant inhibition of the growth, metastasis and self-renewal of OC cells. Mechanistically, THOR drives OC cell progression via the STAT3 signaling. Moreover, the specific STAT3 inhibitor S3I-201 diminished the discrepancy in the growth, metastatic and self-renewal capacity between THOR-silenced OC cells and control cells, which further confirmed that STAT3 was required in THOR-driven OC cells progression.Conclusion Our findings revealed that THOR could promote OC cells growth, metastasis and self-renew by activating STAT3 signaling and may be a good predictive factor and therapeutic target.

scholarly journals Preeclampsia and Keap1 (rs11085735) variants and lncRNA MEG3 methylation status: Association with lncRNA MEG3 hypermethylation

2021 ◽  
Author(s):  
Maryam Zangeneh ◽  
Sara Heydarian ◽  
Zahra Seifi ◽  
Maryam Kohsari ◽  
Zohreh Rahimi
Keyword(s):  
Total Bilirubin ◽  
Late Onset ◽  
Methylation Status ◽  
Normal Pregnancy ◽  
Severe Form ◽  
Normal Weight ◽  
Non Coding Rna ◽  
Significant Difference ◽  
Long Non Coding Rna

Abstract Background. Preeclampsia (PE) is one of the complications of pregnancy. Genetic and epigenetic mechanisms are involved in the preeclampsia pathophysiology. The aims of present study were to investigate the role of Keap1 (rs11085735) variants and the methylation status of long non-coding RNA-maternally expressed gene 3 (lncRNA MEG3) in the pathogenesis of PE in a population from Western Iran with Kurdish ethnic background.Results. There was no significant difference in the frequency of Keap1 genotypes comparing 75 patients with PE and 75 women with normal pregnancy. The frequencies of hemi methylated and full methylated lnc-MEG3 were 94 and 6% (P=0.04), respectively in all patients (50 women), 86.4, and 13.6% (P=0.04), respectively in patients with severe preeclampsia and 98 and 0% in controls (50 women). The frequency of full methylated lnc-MEG3 was 14.3% in early-onset and 2.8% in late-onset preeclampsia (P=0.12). The frequency of full methylated lnc-MEG3 was higher in patients with BMI >25 kg/m2 compared to normal weight patients. The PE patients had significantly higher levels of liver biomarkers (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total bilirubin) and significantly lower platelet count than healthy pregnant women. Conclusions. Hypermethylation status of lnc-MEG3 increased in patients with PE compared to controls that could be contributed in the pathogenesis and development of preeclampsia and its severe form. However, Keap1 variants might not be involved in the pathogenesis of preeclampsia.

scholarly journals SP1 induced Long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A 

2020 ◽  
Author(s):  
Hao Ji ◽  
Juan Wang ◽  
Binbin Lu ◽  
Juan Li ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Molecular Mechanism ◽  
Cell Lines ◽  
Mrna Degradation ◽  
Biological Role ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Regulate Gene

Abstract Background: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration. Methods:We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1. Results:AGAP2-AS1 was significantly upregulated in CCA tumor tissues.SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.

scholarly journals The Role of lncRNA PCAT6 in Cancers

2021 ◽  
Vol 11 ◽  
Author(s):  
Siying Wang ◽  
Zhenyao Chen ◽  
Jingyao Gu ◽  
Xin Chen ◽  
Zhaoxia Wang
Keyword(s):  
Breast Cancer ◽  
Prognostic Biomarker ◽  
Malignant Tumors ◽  
Vital Role ◽  
Cancer Breast ◽  
Non Coding Rna ◽  
Different Types ◽  
Cancer Côlon ◽  
Long Non Coding Rna

Long non-coding RNA (lncRNA) PCAT6 is a member of the Prostate Cancer Associated Transcripts family of molecules. In this review, we focus on the latest studies involving PCAT6 in the diagnosis, treatment, and prognosis of malignant tumors of the digestive, respiratory, urinary, reproductive, motion, and nervous systems. PCAT6 was found to be highly expressed in gastric cancer, colon cancer, hepatocellular carcinoma, lung cancer, bladder cancer, ovarian cancer, breast cancer, cervical cancer, osteosarcoma, glioblastoma, and other tumors. PCAT6 can promote the development and progression of different types of malignant tumors through various mechanisms. Overall, these findings suggest that PCAT6 may play an increasingly vital role in the clinical assessment of these malignant tumors. It can function as an oncogene and may be used as a potential new prognostic biomarker of these tumors.

scholarly journals Long non-coding RNA THOR promotes Ovarian Cancer cells progression via IL-6/STAT3 pathway

2020 ◽  
Author(s):  
Jing Ge ◽  
Tao Han ◽  
Lili Shan ◽  
Jing Na ◽  
Ya Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Malignant Tumors ◽  
Ovarian Cancer Cells ◽  
Self Renewal ◽  
Stat3 Signaling ◽  
Non Coding Rna ◽  
The Impact ◽  
Long Non Coding Rna

Abstract Background: Ovarian cancer (OC) is one of the most common malignant tumors in the world. The prognosis of OC remains poor due to the advanced stage and distant metastasis at the time of diagnosis. Recently, a novel lncRNA, THOR (testis-associated highly conserved oncogenic long non-coding RNA), was characterized in human cancers and shown to exhibit an oncogenic role. However, the role of THOR in OC remains unclear. Methods: RT-PCR and western blot analysis were used to detect the expression of THOR, p-STAT3 and IL-6. The impact of THOR on OC proliferation, metastasis and self-renewal was investigated in vitro and in vivo. The prognostic value of THOR was determined in OC patient cohorts. Results: In this study, our results find that THOR is markedly upregulated in human OC tissues and predicts the poor prognosis of OC patients. Functional studies have revealed that knockdown of THOR inhibits the growth, metastasis and self-renewal of OC cells. Mechanistically, THOR drives OC cell progression via the IL-6/STAT3 signaling. Moreover, the specific STAT3 inhibitor S3I-201 or IL-6R inhibitor tocilizumab diminish the discrepancy in the growth, metastatic and self-renewal capacity between THOR-silenced OC cells and control cells, which further confirm that IL-6/STAT3 is required in THOR-driven OC cells progression. Conclusion: Our findings reveal that THOR could promote OC cells growth, metastasis and self-renewal by activating IL-6/STAT3 signaling and may be a good predictive factor and therapeutic target.

scholarly journals LINC01605, regulated by the EP300-SMYD2 complex, potentiates the binding between METTL3 and SPTBN2 in colorectal cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Meng Yue ◽  
Tao Liu ◽  
Guoqiang Yan ◽  
Xiaofan Luo ◽  
Lei Wang
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Potential ◽  
Rna Seq ◽  
Related Factors ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Tumor Related Death ◽  
Validation Experiments

Abstract Background Colorectal cancer (CC) is one of the major contributors to tumor-related death worldwide, and its main cause of death is distant metastasis. Dysregulation of long non-coding RNA (lncRNA) LINC01605 has been implicated in CC. However, its role in metastasis of CC remains elusive. The goal of the study is to uncover the biological function and molecular mechanism of LINC01605 in CC. Methods The differentially expressed lncRNAs were first screened from GSE97300, GSE84983, GSE110715, GSE70880, and GSE75970 microarrays. The correlation between the expression of LINC01605 and the clinical phenotypes of enrolled CC patients (n = 134) was subsequently analyzed. The upstream and downstream regulatory mechanisms of LINC01605 in CC were identified through bioinformatics and RNA-seq analyses. Finally, the effects of related factors on CC cell growth and metastasis were confirmed through functional validation experiments. Results LINC01605, significantly highly expressed in CC, was a prognostic factor for patients with CC. Functional experiments revealed that LINC01605 knockdown inhibited the proliferatory and metastatic potential of CC cells in vitro and in vivo. Moreover, LINC01605 was regulated by SMYD2-EP300-mediated modifications of histone H3K4me3 as well as H3K27ac. LINC01605 was found to bind to METTL3 and promote the m6A modification of SPTBN2 mRNA, thereby facilitating the translation of SPTBN2. Conclusions Overexpression of LINC01605, regulated by SMYD2-EP300-mediated H3K27ac and H3K4me3 modifications, bound to METTL3 protein to promote m6A modification of SPTBN2 mRNA, leading to the development of CC.

scholarly journals LncRNA STXBP5-AS1 suppresses stem cell-like properties of pancreatic cancer by epigenetically inhibiting neighboring androglobin gene expression

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Shi Chen ◽  
Long Huang ◽  
Ge Li ◽  
Funan Qiu ◽  
Yaodong Wang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Annexin V ◽  
Non Coding Rna ◽  
Rna Immunoprecipitation ◽  
Sphere Formation ◽  
Long Non Coding Rna

Abstract Previous studies suggest the tumor suppressor role of long non-coding RNA (lncRNA) STXBP5-AS1 in cervical and gastric cancer, but its expression pattern and functional mechanism are still elusive in pancreatic cancer (PC). Relative expression of STXBP5-AS1 in PC both in vivo and in vitro was analyzed by real-time PCR. IC50 of Gemcitabine was determined by the MTT assay. Cell proliferation in response to drug treatment was investigated by colony formation assay. Cell apoptosis was measured by both caspase-3 activity and Annexin V/PI staining. Cell invasion capacity was scored by the transwell assay in vitro, and lung metastasis was examined with the tail vein injection assay. Cell stemness was determined in vitro by sphere formation and marker profiling, respectively, and in vivo by limited dilution of xenograft tumor incidence. Subcellular localization of STXBP5-AS1 was analyzed with fractionation PCR. Association between STXBP5-AS1 and EZH2 was investigated by RNA-immunoprecipitation. The binding of EZH2 on ADGB promoter was analyzed by chromatin immunoprecipitation. The methylation was quantified by bisulfite sequencing. We showed downregulation of STXBP5-AS1 in PC associated with poor prognosis. Ectopic STXBP5-AS1 inhibited chemoresistance and metastasis of PC cells. In addition, STXBP5-AS1 compromised stemness of PC cells. Mechanistically, STXBP5-AS1 potently recruited EZH2 and epigenetically regulated neighboring ADGB transcription, which predominantly mediated the inhibitory effects of STXBP5-AS1 on stem cell-like properties of PC cells. Our study highlights the importance of the STXBP5-EZH2-ADGB axis in chemoresistance and stem cell-like properties of PC.

scholarly journals Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Changru Fan ◽  
Qiulan Yuan ◽  
Guifeng Liu ◽  
Yuliang Zhang ◽  
Maojun Yan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Malignant Tumors ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Western Blot Assay ◽  
Resistance Response ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Long Non Coding Rna

Abstract Background Colorectal cancer (CRC) is one of the most general malignant tumors. Accumulating evidence implied that long non-coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) participated in the tumorigenesis of CRC. However, the effect of MALAT1 in drug-resistance needed to be further illustrated. Methods Levels of MALAT1, microRNA (miR)-324-3p, and a disintegrin and metalloprotease metallopeptidase domain 17 (ADAM17) were detected using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit 8 (CCK-8) was used to assess the half maximal inhibitory concentration (IC50) of oxaliplatin (Ox). Meanwhile, cell proliferation, migration and apoptosis were detected by CCK-8, transwell assay, and flow cytometry, respectively. The interaction between miR-324-3p and MALAT1 or ADAM17 was clarified by dual-luciferase reporter assay. Also, the effect of MALAT1 on tumor growth was detected in xenograft tumor mice treated with Ox. Results Significant up regulation of MALAT1 and ADAM17, and decrease of miR-324-3p were observed in Ox-resistant CRC tissues and cells. MALAT1 deficiency enhanced the sensitivity of Ox-resistant CRC cells response to Ox, while miR-324-3p repression or ADAM17 acceleration could overturn this effect. Moreover, MALAT1 silencing repressed tumor growth in Ox-treated nude mice. Mechanically, MALAT1 exerted promotion effect on the resistance response to Ox via miR-324-3p/ADAM17 axis in Ox-resistant CRC cells. Conclusion MALAT1 modulated the sensitivity of Ox through ADAM17 in Ox-resistant CRC cells by sponging miR-324-3p, thus MALAT1 might serve as a novel insight for the therapy of CRC.

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