scholarly journals Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Bo Liu ◽  
Hongyan Zhao ◽  
Lili Zhang ◽  
Xuefeng Shi
Keyword(s):  
Signalling Pathway ◽  
Migration And Invasion ◽  
Transfected Cells ◽  
Non Coding Rna ◽  
Mapk Signalling ◽  
U2os Cells ◽  
Umr 106 ◽  
Long Non Coding Rna ◽  
E Cadherin

Abstract Background Osteosarcoma (OS) is a malignancy of the bone that has no clearly identified prognostic factors for diagnosis. In this study, we evaluated the regulatory role of long non-coding RNA (lncRNA) ANCR on the migration and invasion of OS cells as well as the possible mechanism involving the p38MAPK signalling pathway. Methods ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR. It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection. The proliferation of transfected cells was determined using the CCK-8 and the EdU assays. The migration and invasion of transfected cells were determined by the Transwell assay. The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by Western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells. Results ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCR-induced inhibition of cell migration and invasion. Conclusions Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.

scholarly journals LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression

2021 ◽  
Vol 16 (1) ◽  
pp. 1-13
Author(s):  
Weiwei Liu ◽  
Dongmei Yao ◽  
Bo Huang
Keyword(s):  
Cervical Cancer ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Western Blot Assay ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.

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 CASC2 regulates cell biological behaviour through the MAPK signalling pathway in hepatocellular carcinoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (6) ◽  
pp. 101042831770622 ◽  
Author(s):  
Yuanyuan Gan ◽  
Nana Han ◽  
Xiaoqin He ◽  
Jiajun Yu ◽  
Meixia Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signalling Pathway ◽  
Biological Behaviour ◽  
Mapk Signalling Pathway ◽  
Non Coding Rna ◽  
Mapk Signalling ◽  
Long Non Coding Rna

Silencing of Long Non-Coding RNA Myocardial Infarction-Associated Transcript Suppresses Progression of Gastric Cancer

2019 ◽  
Vol 9 (5) ◽  
pp. 637-645
Author(s):  
Lei Wang ◽  
Qi Hu ◽  
Feng Gu
Keyword(s):  
Gastric Cancer ◽  
G1 Phase ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Cycle Arrest ◽  
Non Coding Rna ◽  
Cox 2 ◽  
Cell Arrest ◽  
Long Non Coding Rna

Background: Long noncoding RNAs (lncRNAs) have been consistently demonstrated to be involved in gastric cancer (GC) as either tumor oncogenes or tumor suppressors. However, the detailed role of MIAT in GC remains poorly understood. Methods: The expression of MIAT in GC tissues was measured by In situ hybridization (ISH) assay. Cell proliferation, apoptosis, cycle, migration and invasion assays were performed to analyze the biological functions of MIAT in GC cells. Besides, western blotting was used to evaluate the role of MIAT in the expressions of P16, COX-2 and MMP-9. Results: In the present study, we identified that MIAT was up-regulated in GC tissues. Furthermore, silencing MIAT significantly suppressed GC cells proliferation, migration and invasion, promoted GC cells apoptosis, and induced GC cells cycle arrest in G1 phase. Additionally, knockdown of MIAT notably up-regulated the protein level of P16 and down-regulated the protein levels of COX-2 and MMP-9. Conclusion: These observations imply that silencing MIAT inhibits the proliferation, migration and invasion, promotes apoptosis, and induces cell arrest in G1 phase, partially through up-regulating the expression level of P16 and down-regulating the expression levels of COX-2 and MMP-9, indicating that MIAT may a novel biomarker and therapeutic target for GC.

scholarly journals The Long Non-Coding RNA Prader Willi/Angelman Region RNA5 (PAR5) Is Downregulated in Anaplastic Thyroid Carcinomas Where It Acts as a Tumor Suppressor by Reducing EZH2 Activity

Cancers ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 235 ◽  
Author(s):  
Simona Pellecchia ◽  
Romina Sepe ◽  
Myriam Decaussin-Petrucci ◽  
Cristina Ivan ◽  
Masayoshi Shimizu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Tumor Suppressor ◽  
Cell Lines ◽  
Cancer Progression ◽  
P Value ◽  
Thyroid Carcinomas ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
E Cadherin

Anaplastic thyroid carcinoma (ATC) represents one the most aggressive neoplasias in humans, and, nowadays, limited advances have been made to extend the survival and reduce the mortality of ATC. Thus, the identification of molecular mechanism underlying its progression is needed. Here, we evaluated the long non-coding RNA (lncRNA) expression profile of nine ATC in comparison with five normal thyroid tissues by a lncRNA microarray. By this analysis, we identified 19 upregulated and 28 downregulated lncRNAs with a fold change >1.1 or <−1.1 and p-value < 0.05, in ATC samples. Some of them were subsequently validated by qRT-PCR. Then, we investigated the role of the lncRNA Prader Willi/Angelman region RNA5 (PAR5), drastically and specifically downregulated in ATC. The restoration of PAR5 reduces proliferation and migration rates of ATC-derived cell lines indicating that its downregulation contributes to thyroid cancer progression. Our results suggest that PAR5 exerts its anti-oncogenic role by impairing Enhancer of Zeste Homolog 2 (EZH2) oncogenic activity since we demonstrated that PAR5 interacts with it in thyroid cancer cell lines, reducing EZH2 protein levels and its binding on the E-cadherin promoter, relieving E-cadherin from the negative regulation by EZH2. Consistently, EZH2 is overexpressed in ATC, but not in differentiated thyroid carcinomas. The results reported here define a tumor suppressor role for PAR5 in undifferentiated thyroid neoplasias, further highlighting the pivotal role of lncRNAs in thyroid carcinogenesis.

Long non-coding RNA PHACTR2-AS1 promotes tongue squamous cell carcinoma metastasis by regulating Snail

2020 ◽  
Vol 168 (6) ◽  
pp. 651-657 ◽  
Author(s):  
Fenqian Yuan ◽  
Zhiguo Miao ◽  
Wen Chen ◽  
Fanggeng Wu ◽  
Chao Wei ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Biology ◽  
Tongue Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Long non-coding RNA is an endogenous non-coding RNA that has currently been proved to be an important player in cancer cell biology. In the present study, we investigated the biological role of PHACTR2-AS1 in tongue squamous cell carcinoma (TSCC). PHACTR2-AS1 was preferentially localized in the cytoplasm, and was notably upregulated in TSCC tissues. High PHACTR2-AS1 was correlated with tumour differentiation, metastatic clinical features, relapse and shortened survival time. Depletion of PHACTR2-AS1 did not affect TSCC cell viability and colony formation ability, whereas substantially inhibited cell migration and invasion in vitro and lung metastasis in vivo. Mechanistically, PHACTR2-AS1 could sponge miR-137 to increase Snail expression, resulting in triggering epithelial–mesenchymal transition process, thereby promoting TSCC cell metastasis. Taken together, our data for the first time elucidate the metastasis-promoting role of PHACTR2-AS1 in TSCC, hinting a new therapeutic target for metastatic TSCC patients.

scholarly journals Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shengjie Yu ◽  
Huihong Yu ◽  
Yuanfeng Zhang ◽  
Chuan Liu ◽  
Weili Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
The Relationship ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. Methods qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. Results LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. Conclusion Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.

scholarly journals Long non-coding RNA SNHG6 promotes tumorigenesis of nasopharyngeal carcinoma by competitively binding to miR-944 with RGS17

2020 ◽  
Author(s):  
Yu’e Han ◽  
Xing Liu ◽  
Guangling Li ◽  
Xia Ju ◽  
Zhongyi Song
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Regulatory Mechanism ◽  
Suppressive Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Reporter Assays ◽  
Direct Target ◽  
Long Non Coding Rna

Abstract Background Previous studies have shown that many long noncoding RNAs (lncRNAs) are involved in the pathogenesis of nasopharyngeal carcinoma (NPC). However, the regulatory mechanism of lncRNA SNHG6 remains unknown. Therefore, this study was design to preliminarily elucidate the role of SNHG6 in NPC. Methods The mRNA expression was detected by RT-qPCR. CCK-8, Transwell and dual luciferase reporter assays were used to investigate the function of SNHG6 in NPC. Results Upregulation of SNHG6 and downregulation of miR-944 were identified in NPC and were associated with TNM stage and distant metastasis in NPC patients. Additionally, SNHG6 acts as a molecular sponge of miR-944. More importantly, SNHG6 promoted NPC cell proliferation, migration and invasion by downregulating miR-944. Further, RGS17 was confirmed to be a direct target of miR-944. MiR-944 restrained NPC progression by targeting RGS17. Besides that, knockdown of RGS17 was found to block NPC progression. Upregulation of SNHG6 weakened the suppressive effect of RGS17 knockdown in NPC. Conclusion LncRNA SNHG6 promotes tumorigenesis of NPC by competitively binding to miR-944 with RGS17.

scholarly journals LncRNA HOTAIR regulates the expression of E-cadherin to affect nasopharyngeal carcinoma progression by recruiting histone methylase EZH2 to mediate H3K27 trimethylation

2019 ◽  
Author(s):  
Feng-lian Yang ◽  
Yu-xia Wei ◽  
Bi-yun Liao ◽  
Gui-jiang Wei ◽  
Hai-mei Qin ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Clinicopathological Characteristics ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Non Coding Rna ◽  
Promote Cell Migration ◽  
Ezh2 Expression ◽  
Long Non Coding Rna ◽  
Lncrna Hotair ◽  
E Cadherin

Abstract Background In recent years, there has been increasing evidence for the function of long non-coding RNA (lncRNA) in nasopharyngeal carcinoma (NPC).. We aim to delve into the position of lncRNA HOTAIR, together with EZH2, E-cadherin and H3K27me3 in NPC and explore the related mechanisms. Methods RT-qPCR and western blot analysis were carried out for detecting lncRNA HOTAIR, EZH2, E-cadherin and H3K27me3 expression in NPC tissues and cells. Moreover, the correlations between lncRNA HOTAIR and EZH2 expression and the clinicopathological characteristics and prognosis of patients with NPC were observed. NPC cell biological functions were examined through gain-of and loss-of function assays. RIP and ChIP assays were applied to detect whether lncRNA HOTAIR in NPC cells could regulate E-cadherin by recruiting EZH2 to mediate trimethylation of H3K27. Results LncRNA HOTAIR, EZH2, and H3K27me3 were richly expressed in NPC tissues and cells, and E-cadherin was lowly expressed. The prognosis of patients with overexpression of lncRNA HOTAIR and EZH2 was worse than that of patients with theirs low expression. Down-regulation of either HOTAIR or EZH2 inhibited cell proliferation, promoted apoptosis, suppressed migration and invasion and inhibited tumor growth. HOTAIR recruited histone methylase EZH2 to mediate trimethylation of H3K27 and regulated E-cadherin expression. Conclusion Our study suggests that lncRNA HOTAIR inhibits the expression of E-cadherin by stimulating the trimethylation of H3K27 by histone methylase EZH2 to promote cell migration, proliferation, and inhibit apoptosis of NPC cells.

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