LncRNA ZFAS1, as a poor prognostic indicator, promotes cell proliferation and epithelial–mesenchymal transition in endometrial carcinoma

2020 ◽  
Author(s):  
Yanan Sun ◽  
Xuan Gao ◽  
Peiling Li ◽  
Ling Song ◽  
Lei Shi
Keyword(s):  
Endometrial Carcinoma ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Histological Grade ◽  
Myometrial Invasion ◽  
Migration And Invasion ◽  
Factor X ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
Gynecology And Obstetrics

Background: Long noncoding RNA Zinc finger nuclear transcription factor, X-box binding 1-type containing 1 antisense RNA 1 (ZFAS1) has been reported to be an oncogene in various tumors. However, the role of ZFAS1 in endometrial carcinoma (EC) are not fully determined. Methods & results: Here, we found ZFAS1 expression was significantly upregulated in EC patients, which was significantly associated with International Federation of Gynecology and Obstetrics stage, histological grade, myometrial invasion and poor prognosis. The loss-of-function assays showed that knockdown of ZFAS1 significantly suppressed the proliferation, G1/S transition, migration and invasion in EC cells. Moreover, knockdown of ZFAS1 obviously downregulated the expression of CDK4, Cyclin D1 and N-cadherin, but upregulated E-cadherin expression. Conclusion: Collectively, these results suggest that ZFAS1 might be used as potential therapeutic targets for EC treatment.

scholarly journals LncRNA ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of lung adenocarcinoma

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Rong-Hang Hu ◽  
Zi-Teng Zhang ◽  
Hai-Xiang Wei ◽  
Lu Ning ◽  
Jiang-Shan Ai ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Mesenchymal Transition

Abstract Background Growing evidence suggests that suppressor of tumorigenicity 7 antisense RNA 1 (ST7-AS1) is an oncogenic long noncoding RNA (lncRNA). However, little is known on its clinical significance, biological functions, or molecular mechanisms in lung adenocarcinoma (LUAD). Methods The expression of ST7-AS1 and miR-181b-5p were examined by qRT-PCR. The correlations between ST7-AS1 level and different clinicopathological features were analysed. In vitro, LUAD cells were examined for cell viability, migration and invasion by MTT, wound healing and Transwell assay, respectively. Epithelial-mesenchymal transition (EMT) biomarkers were detected by Western blot. The regulations between ST7-AS1, miR-181b-5p, and KPNA4 were examined by luciferase assay, RNA immunoprecipitation, RNA pulldown. Both gain- and loss-of-function strategies were used to assess the importance of different signalling molecules in malignant phenotypes of LUAD cells. The in vivo effect was analysed using the xenograft and the experimental metastasis mouse models. Results ST7-AS1 was upregulated in LUAD tissues or cell lines, correlated with tumours of positive lymph node metastasis or higher TNM stages, and associated with shorter overall survival of LUAD patients. ST7-AS1 essentially maintained the viability, migration, invasion, and EMT of LUAD cells. The oncogenic activities of ST7-AS1 were accomplished by sponging miR-181b-5p and releasing the suppression of the latter on KPNA4. In LUAD tissues, ST7-AS1 level positively correlated with that of KPNA4 and negatively with miR-181b-5p level. In vivo, targeting ST7-AS1 significantly inhibited xenograft growth and metastasis. Conclusions ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of LUAD cells. Targeting ST7-AS1 and KPNA4 or up-regulating miR-181b-5p, therefore, may benefit the treatment of LUAD.

scholarly journals Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jie Wang ◽  
Zhiwei He ◽  
Jian Xu ◽  
Peng Chen ◽  
Jianxin Jiang
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Progression ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Loss Of Function ◽  
Mesenchymal Transition

AbstractAn accumulation of evidence indicates that long noncoding RNAs are involved in the tumorigenesis and progression of pancreatic cancer (PC). In this study, we investigated the functions and molecular mechanism of action of LINC00941 in PC. Quantitative PCR was used to examine the expression of LINC00941 and miR-335-5p in PC tissues and cell lines, and to investigate the correlation between LINC00941 expression and clinicopathological features. Plasmid vectors or lentiviruses were used to manipulate the expression of LINC00941, miR-335-5p, and ROCK1 in PC cell lines. Gain or loss-of-function assays and mechanistic assays were employed to verify the roles of LINC00941, miR-335-5p, and ROCK1 in PC cell growth and metastasis, both in vivo and in vitro. LINC00941 and ROCK1 were found to be highly expressed in PC, while miR-335-5p exhibited low expression. High LINC00941 expression was strongly associated with larger tumor size, lymph node metastasis, and poor prognosis. Functional experiments revealed that LINC00941 silencing significantly suppressed PC cell growth, metastasis and epithelial–mesenchymal transition. LINC00941 functioned as a molecular sponge for miR-335-5p, and a competitive endogenous RNA (ceRNA) for ROCK1, promoting ROCK1 upregulation, and LIMK1/Cofilin-1 pathway activation. Our observations lead us to conclude that LINC00941 functions as an oncogene in PC progression, behaving as a ceRNA for miR-335-5p binding. LINC00941 may therefore have potential utility as a diagnostic and treatment target in this disease.

LAPTM4B-35 Overexpression Is an Independent Prognostic Marker in Endometrial Carcinoma

2010 ◽  
Vol 20 (5) ◽  
pp. 745-750 ◽  
Author(s):  
Fan-ling Meng ◽  
Ming-zhu Yin ◽  
Hong-tao Song ◽  
Hua Yang ◽  
Ge Lou ◽  
...  
Keyword(s):  
Overall Survival ◽  
Endometrial Carcinoma ◽  
Cancer Progression ◽  
Histological Grade ◽  
Disease Free Survival ◽  
Myometrial Invasion ◽  
Normal Endometrium ◽  
Free Survival ◽  
Gynecology And Obstetrics ◽  
Disease Free

Background:Lysosomal protein transmembrane 4 β-35 (LAPTM4B-35), a novel oncoprotein that belongs to the mammalian 4-tetratransmembrane spanning protein superfamily, has been implicated in oncogenesis and cancer progression in several solid malignances. However, the expression of LAPTM4B-35 and its role in endometrial cancer progression remain unknown.Materials and Methods:We investigated the expression of the LAPTM4B-35 protein by immunohistochemistry in 30 normal endometrium specimens and 165 endometrial carcinomas and analyzed its correlation with various clinicopathologic features, including patient outcome.Results:LAPTM4B-35 immunoreactivity was overexpressed in endometrial carcinoma cases compared with normal endometrium (P < 0.001). High LAPTM4B-35 expression was found in 117 (70.91%) of these 165 carcinomas and was positively correlated with the International Federation of Gynecology and Obstetrics stage, histological grade, depth of myometrial invasion, lymph node metastasis, lymph vascular space involvement, and recurrence, but not with age and histological type. Patients with high LAPTM4B-35 expression had significantly poorer overall survival and disease-free survival compared with patients with low expression of LAPTM4B-35 (P = 0.001 and P = 0.002, respectively). Multivariate analysis showed that high LAPTM4B-35 expression was an independent prognostic factor for both overall survival and disease-free survival of patients with endometrial carcinoma (both P = 0.005).Conclusions:These results showed that high LAPTM4B-35 expression was associated with progression and prognosis of endometrial carcinoma.

scholarly journals lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

2018 ◽  
Vol 48 (5) ◽  
pp. 1928-1941 ◽  
Author(s):  
Chuan He ◽  
Zhigang Liu ◽  
Li Jin ◽  
Fang Zhang ◽  
Xinhao Peng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Noncoding Rna ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

scholarly journals Upregulation of long noncoding RNA zinc finger antisense 1 enhances epithelial–mesenchymal transition in vitro and predicts poor prognosis in glioma

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769502 ◽  
Author(s):  
Qiao-Li Lv ◽  
Shu-Hui Chen ◽  
Xue Zhang ◽  
Bao Sun ◽  
Lei Hu ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cox Regression ◽  
Epithelial Mesenchymal Transition ◽  
Clinical Stage ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Cox Regression Analysis ◽  
High Zinc

Increasing evidence indicates that long noncoding RNAs play important roles in development and progression of various cancers. Zinc finger antisense 1 is a novel long noncoding RNA whose clinical significance, biological function, and underlying mechanism are still undetermined in glioma. In this study, we reported that zinc finger antisense 1 expression was markedly upregulated in glioma and tightly correlated with clinical stage. Moreover, patients with high zinc finger antisense 1 expression had shorter survival. Multivariate Cox regression analysis provided a clue that, probably, zinc finger antisense 1 level could serve as an independent prognostic factor for glioma. Functionally, zinc finger antisense 1 acted as an oncogene in glioma because its knockdown could promote apoptosis and significantly inhibit cell proliferation, migration, and invasion. Furthermore, zinc finger antisense 1 silencing could result in cell cycle arrest at the G0/G1 phase and correspondingly decrease the percentage of S phase cells in both U87 and U251 cell lines. Moreover, it was found that silenced zinc finger antisense 1 could impair migration and invasion by inhibiting the epithelial–mesenchymal transition through reducing the expression of MMP2, MMP9, N-cadherin, Integrin β1, ZEB1, Twist, and Snail as well as increasing E-cadherin level in glioma. Taken together, our data identified that zinc finger antisense 1 might act as a valuable prognostic biomarker and potential therapeutic target for glioma.

scholarly journals STAT3α Is Oncogenic for Endometrial Carcinoma Cells and Mediates the Oncogenic Effects of Autocrine Human Growth Hormone

Endocrinology ◽  
2010 ◽  
Vol 151 (9) ◽  
pp. 4133-4145 ◽  
Author(s):  
Jian-Zhong Tang ◽  
Xiang-Jun Kong ◽  
Arindam Banerjee ◽  
Nethaji Muniraj ◽  
Vijay Pandey ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Small Interfering Rna ◽  
Epithelial Mesenchymal Transition ◽  
Dominant Negative ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Stat3 Phosphorylation ◽  
Ec Cells ◽  
Interfering Rna

We herein demonstrate an oncogenic role for signal transducer and activator of transcription (STAT)-3α (the full length STAT3 isoform), which also mediates autocrine human GH (hGH)-stimulated oncogenicity, in human endometrial carcinoma (EC) cells. Autocrine hGH stimulated Y705 phosphorylation of STAT3 and STAT3-mediated transcriptional activity in a SRC and Janus-2 Kinase dependent manner in human EC cell lines. Forced expression of a constitutively active variant of STAT3α increased proliferation, anchorage-independent, three-dimensional (3D) Matrigel, and xenograft growth and promoted epithelial-mesenchymal transition, migration, and invasion of EC cells. Conversely, the oncogenic capacity of EC cells was significantly impaired by treatment with JSI-124, an inhibitor of STAT3 phosphorylation and activity, small interfering RNA-mediated depletion of STAT3α, or a dominant-negative variant of STAT3α. Furthermore, the enhanced EC cell oncogenicity stimulated by autocrine hGH, was also abrogated by functional inhibition or small interfering RNA-mediated depletion of STAT3α. STAT3α may therefore be a common mediator of oncogenic signaling pathways stimulating progression of EC.

FOXD2-AS1 promotes migration and invasion of head and neck squamous cell carcinoma and predicts poor prognosis

2020 ◽  
Vol 16 (28) ◽  
pp. 2209-2218
Author(s):  
Li Zhang ◽  
Hao Bo ◽  
Tingwei Chen ◽  
Qiaohua Li ◽  
Ye Huan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Neck Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Aim: To investigate the role of long noncoding RNA FOXD2-AS1 in head and neck squamous cell carcinoma (HNSCC). Materials & methods: The expression and clinical significance of FOXD2-AS1 were analyzed using data from public databases. Transwell assays were used to examine the function of FOXD2-AS1 in HNSCC. The molecular mechanism of FOXD2-AS1 was probed by western blotting. Results: The expression of FOXD2-AS1 was upregulated in HNSCC; it was positively related with the pathological stage as well as with poor prognosis in HNSCC patients. FOXD2-AS1 silencing inhibited HNSCC cell migration and invasion, also influenced the expression of epithelial–mesenchymal transition-related molecules. Conclusion: FOXD2-AS1 was a prognostic marker in patients with HNSCC and may be a favorable novel treatment target for HNSCC.

Expression of lncRNA TINCR in the placenta of patients with pre-eclampsia and its effect on the biological behaviours of trophoblasts

Zygote ◽  
2021 ◽  
pp. 1-9
Author(s):  
Li Qin ◽  
Qin Yang ◽  
Zhiyi Fei ◽  
Dandan Zhang
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Terminal Differentiation ◽  
S Phase ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Protein Coding ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Related Proteins

Summary To explore the effect of lncRNA TINCR on the biological behaviours of trophoblasts, we detected and analyzed the expression of terminal differentiation-induced non-protein coding RNA (TINCR) in the placenta tissues of pre-eclamptic and non-pre-eclamptic pregnant women. The gain- and loss-of-function of TINCR was performed to examine the proliferation, migration and invasion abilities of Htr-8/Svneo cells. The levels of epithelial–mesenchymal transition (EMT)-related proteins, cyclin and Wnt/β-catenin pathway were detected. High expression of lncRNA TINCR appeared in placental tissues of patients with pre-eclampsia. The proliferation, invasion and migration of Htr-8/Svneo cells were promoted by TINCR downregulation; the cells were transited from G0/G1 to S phase; and EMT was promoted and the Wnt/β-catenin pathway was activated. In summary, the downregulation of lncRNA TINCR activated the Wnt/β-catenin pathway and promoted the proliferation, invasion and migration of Htr-8/Svneo cells. This study may provide a theoretical basis for treatment of patients with pre-eclampsia.

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