The tumor suppressive effect of long non-coding RNA FRMD6-AS2 in uteri corpus endometrial carcinoma

Abstract Background Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma, lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. Methods We used qRT-PCR to detect the expression of MONC, miR-636 and GLCE in normal human endometrial tissues and endometrial carcinoma tissues. Luciferase assay was used to verify the binding sites between MONC and miR-636 and between miR-636 and GLCE. The double fluorescence in situ hybridization was used to locate MONC and miR-636 in cells. Endometrial cancer stem cells were obtained by Flow cytometry sorting assay. Sphere formation assay, CCK-8 assay, transwell invasion assay, cell cycle analysis and apoptosis assay were used to detect the effects of MONC/miR-636/GLCE axis on the malignant biological behavior of ECSCs and endometrial carcinoma cells (ECCs). The effect of MONC on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Finally, we conducted in vivo verification through Tumor xenografts in nude mice. Results In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. We found MONC is low expression in endometrial carcinoma (EC), MONC and miR-636 are relatively co-localized in the cytoplasm. MONC directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3'-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC. Conclusions In conclusion, this study shows that MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. The MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.

Download Full-text

Long Non-Coding RNA SNHG14 Impedes Viability, Migration and Invasion of Endometrial Carcinoma Cells Through Modulating miR-93-5p/ZBTB7A Axis

Cancer Management and Research ◽

10.2147/cmar.s257419 ◽

2020 ◽

Vol Volume 12 ◽

pp. 9515-9525

Author(s):

Kai Zhang ◽

Yongqin Cai ◽

Qi Zhou ◽

Hong Sun ◽

Jinying Wei

Keyword(s):

Endometrial Carcinoma ◽

Carcinoma Cells ◽

Migration And Invasion ◽

Non Coding Rna ◽

Long Non Coding Rna

Download Full-text

Long non-coding RNA tumor suppressor candidate 7 advances chemotherapy sensitivity of endometrial carcinoma through targeted silencing of miR-23b

Tumor Biology ◽

10.1177/1010428317707883 ◽

2017 ◽

Vol 39 (6) ◽

pp. 101042831770788 ◽

Cited By ~ 13

Author(s):

Chao Shang ◽

Bin Lang ◽

Cheng Ngok Ao ◽

Lirong Meng

Keyword(s):

Tumor Suppressor ◽

Endometrial Carcinoma ◽

Chemotherapy Sensitivity ◽

Non Coding Rna ◽

Long Non Coding Rna

Download Full-text

LncRNA MONC suppresses the malignant phenotype of Endometrial Cancer Stem Cells and Endometrial Carcinoma Cells by regulating the MiR-636/GLCE axis

Cancer Cell International ◽

10.1186/s12935-021-01911-1 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yibing Li ◽

Jianing Huo ◽

Junjian He ◽

Xiaoxin Ma

Keyword(s):

Stem Cells ◽

Endometrial Cancer ◽

Cancer Stem Cells ◽

Endometrial Carcinoma ◽

Nude Mice ◽

Epithelial To Mesenchymal Transition ◽

Suppressive Effect ◽

Biological Behavior ◽

Mesenchymal Transition ◽

Tumor Suppressive Effect

Abstract Background Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma, lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. Methods We used qRT-PCR to detect the expression of MONC, miR-636 and GLCE in normal human endometrial tissues and endometrial carcinoma (EC) tissues. Luciferase assay was used to verify the binding sites between MONC and miR-636 and between miR-636 and GLCE. Double fluorescence in situ hybridization was used to locate MONC and miR-636 in cells. ECSCs were obtained by flow cytometry sorting assay. Sphere formation assay, CCK-8 assay, transwell invasion assay, cell cycle analysis and apoptosis assay were used to detect the effects of MONC/miR-636/GLCE axis on the malignant biological behavior of ECSCs and ECCs. The effect of MONC on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Finally, we conducted in vivo verification through Tumor xenografts in BALB/C nude mice. Results In this study, we found MONC is low expression in endometrial carcinoma (EC) and patients in the MONC high-expression group had a better prognosis. MONC and miR-636 are relatively co-localized in the cytoplasm. MONC directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3′-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC. Conclusions In conclusion, this study showed that MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. Thus the MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.

Download Full-text

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

10.21203/rs.3.rs-25032/v1 ◽

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.

Download Full-text

Long non-coding RNA MCM3AP-AS1 promotes growth and migration through modulating FOXK1 by sponging miR-138-5p in pancreatic cancer

Molecular Medicine ◽

10.1186/s10020-019-0121-2 ◽

2019 ◽

Vol 25 (1) ◽

Cited By ~ 4

Author(s):

Ming Yang ◽

Shijuan Sun ◽

Yao Guo ◽

Junjie Qin ◽

Guangming Liu

Keyword(s):

Pancreatic Cancer ◽

Suppressive Effect ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Reporter Assay ◽

Non Coding Rna ◽

And Migration ◽

Long Non Coding Rna ◽

Dual Luciferase Reporter Assay

Abstract Background Pancreatic cancer (PC) is a type of malignant gastrointestinal tumor. Long non-coding RNA MCM3AP antisense RNA 1 (MCM3AP-AS1) has been reported to stimulate proliferation, migration and invasion in several types of tumors. However, the role of MCM3AP-AS1 in PC remains unclear. Methods MCM3AP-AS1, microRNA miR-138-5p (miR-138-5p) and FOXK1 levels were detected using quantitative real time PCR. Cell proliferation, migration and invasion were analyzed. Dual luciferase reporter assay was used to confirm the relationship between MCM3AP-AS1 and miR-138-5p, between miR-138-5p and FOXK1. Protein levels were identified using western blot analysis. Results MCM3AP-AS1 overexpression promoted proliferation, migration and invasion in PC cells. MCM3AP-AS1 silencing showed a suppressive effect on cell growth in PC cells. Moreover, MCM3AP-AS1 knockdown suppressed tumor growth in mice. Dual luciferase reporter assay demonstrated MCM3AP-AS1 could sponge microRNA-138-5p (miR-138-5p), and FOXK1 could bind with miR-138-5p. Positive correlation between MCM3AP-AS1 and FOXK1 was testified, as well as negative correlation between miR-138-5p and FOXK1. MCM3AP-AS1 promoted FOXK1 expression by targeting miR-138-5p, and MCM3AP-AS1 facilitated growth and invasion in PC cells by FOXK1. Conclusion MCM3AP-AS1 promoted growth and migration through modulating miR-138-5p/FOXK1 axis in PC, providing insights into MCM3AP-AS1/miR-138-5p/FOXK1 axis as novel candidates for PC therapy from bench to clinic.

Download Full-text