scholarly journals HOXC6-Mediated miR-188-5p Expression Induces Cell Migration through the Inhibition of the Tumor Suppressor FOXN2

2021 ◽  
Vol 23 (1) ◽  
pp. 9
Author(s):  
Seho Jeong ◽  
Soo-A Kim ◽  
Sang-Gun Ahn
Keyword(s):  
Cell Migration ◽  
Tumor Suppressor ◽  
Cancer Progression ◽  
Regulatory Networks ◽  
Suppressor Gene ◽  
Malignant Progression ◽  
Luciferase Assay ◽  
Regulatory Interactions ◽  
Forkhead Box ◽  
Microarray Profiling

Homeobox C6 (HOXC6) is a transcription factor that plays a role in the malignant progression of various cancers. However, the roles of HOXC6 and its regulatory mechanism remain unclear. In this study, we used microRNA (miRNA) regulatory networks to identify key regulatory interactions responsible for HOXC6-mediated cancer progression. In microarray profiling of miRNAs, the levels of miRNAs such as hsa-miR-188-5p, hsa-miR-8063, and hsa-miR-8064 were significantly increased in HOXC6-overexpressing cells. Higher positive expression rates of HOXC6 and miR-188-5p were observed in malignant cancer. We also found that HOXC6 significantly upregulated miR-188-5p expression. The underlying function of HOXC6-mediated miR-188-5p expression was predicted through TargetScan and the MiRNA Database. Overexpression of mir-188-5p inhibited the expression of forkhead box N2 (FOXN2), a tumor suppressor gene. Furthermore, in the luciferase assay, miR-188-5p bound to the 3′-UTR of FOXN2 and was mainly responsible for the dysregulation of FOXN2 expression. Silencing FOXN2 induced cell migration, and the effect of FOXN2 silencing was enhanced when the HOXC6/miR-188-5p axis was induced. These results suggest that HOXC6/miR-188-5p may induce malignant progression in cancer by inhibiting the activation of the FOXN2 signaling pathway.

scholarly journals Decreased level of miR-1301 promotes colorectal cancer progression via activation of STAT3 pathway

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Fangfang Yang ◽  
Hua Wang ◽  
Bianbian Yan ◽  
Tong Li ◽  
Lulu Min ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Aberrant Expression ◽  
Cell Migration And Invasion ◽  
Lovo Cells ◽  
Colorectal Cancer Progression

Abstract The molecular pathogenesis of colorectal cancer (CRC) has been widely investigated in recent years. Accumulating evidence has indicated that microRNA (miRNA) dysregulation participates in the processes of driving CRC initiation and progression. Aberrant expression of miR-1301 has been found in various tumor types. However, its role in CRC remains to be elucidated. In the present study, we identified miR-1301 was enriched in normal colorectal tissues and significantly down-regulated in CRC. Decreased level of miR-1301 strongly correlated with aggressive pathological characteristics, including advanced stage and metastasis. Bioinformatics and dual luciferase assay demonstrated that STAT3 is a direct target of miR-1301. Gain and loss-of-function assays showed that miR-1301 had no effect on cell proliferation. Overexpression of miR-1301 suppressed cell migration and invasion capacity of pSTA3-positive LoVo cells, but not pSTAT3-negative SW480 cells, while inhibition of miR-1301 consistently promoted cell migration and invasion in both cell lines. Additionally, miR-1301 inhibition restored the suppressed migration and invasion of STAT3- knockdown LoVo cells. MiR-1301 functioned as a tumor suppressor to modulate the IL6/STAT3 signaling pathway. In summary, this study highlights the significant role of miR- 1301/STAT3 axis in CRC metastasis.

scholarly journals Haploinsufficiency of the Pten tumor suppressor gene promotes prostate cancer progression

2001 ◽  
Vol 98 (20) ◽  
pp. 11563-11568 ◽  
Author(s):  
B. Kwabi-Addo ◽  
D. Giri ◽  
K. Schmidt ◽  
K. Podsypanina ◽  
R. Parsons ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cancer Progression ◽  
Suppressor Gene ◽  
Prostate Cancer Progression

scholarly journals MicroRNA-2392 Functions as a Tumor Suppressor Gene and Inhibits Malignant Progression of Hepatocellular Carcinoma via Directly Targeting JAG2

2021 ◽  
Author(s):  
Chunying Liu ◽  
Bin Sun ◽  
Weidan Ji ◽  
Xuejing Lin ◽  
Lei Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Malignant Progression ◽  
Spheroid Formation ◽  
Down Regulation ◽  
Potential Target ◽  
Target Mrnas ◽  
Hcc Cells

Abstract Background Dysregulation of microRNA (miRNA) expression in various cancers and their vital roles in malignant progression of cancers are well investigated. Our previous studies have analyzed miRNAs that promote malignant progression of hepatocellular carcinoma (HCC), this study aim to systematically elucidate metastasis suppressor miRNAs in HCC. Methods High-throughput RNA sequencing analysis was used to identify anti-metastatic miRNAs of HCC. The relative expression levels of miRNAs were confirmed by qRT-PCR. The biological functions of miRNAs were studied by CCK8, wound-healing, transwell, colony formation in HCC cells. Circulating tumor cells were enriched from blood samples of HCC patients and cultured by three-dimensional (3D) system. The potential target mRNAs of miRNAs were analyzed by bioinformatics analysis and confirmed by luciferase reporter assay. Liver metastasis model via tail vein injection was further examined in nude mice. Kaplan-Meier and Cox regression were used to analyze the value of potential target mRNAs on overall survival. Results miR-2392 was significantly down-regulated in HCC. Overexpression of miR-2392 suppressed proliferation, mobility, spheroid formation and maintenance of cancer stem cells (CSC)-like characteristics in HCC cell lines, whereas down-regulation of miR-2392 led to the opposite results. CTCs from HCC patients with lower serum miR-2392 level had stronger cell spheroid formation ability. A negative correlation between the content of miR-2392 in serum and the number of CTC spheroids had been found. We identified Jagged2 (JAG2) as a direct target of miR-2392, miR-2392 inhibited the expression and nuclear accumulation of JAG2 by targeting 3’-UTR of JAG2. HCC cells were treated with LV-miR-2392 inhibitor and JAG2-siRNA to explore the mechanism of miR-2392 and JAG2 on HCC. Down-regulation of JAG2 inhibited the overexpression effects of miR-2392 in vitro and in vivo. JAG2 is highly expressed in HCC and is closely related to poor prognosis and survival of patients. Conclusions Our findings indicated a significant role of the miR-2392/JAG2 axis in suppressing HCC cell growth and aggressiveness, miR-2392 may play a role as a tumor suppressor gene to guide the individualized precise treatment of HCC.

scholarly journals A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability

PLoS Genetics ◽  
2018 ◽  
Vol 14 (11) ◽  
pp. e1007802 ◽  
Author(s):  
Mahdieh Jadaliha ◽  
Omid Gholamalamdari ◽  
Wei Tang ◽  
Yang Zhang ◽  
Ana Petracovici ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cancer Progression ◽  
Mrna Stability ◽  
Suppressor Gene ◽  
Breast Cancer Progression ◽  
Gene Mrna

scholarly journals Molecular networks of FOXP family: dual biologic functions, interplay with other molecules and clinical implications in cancer progression

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Ju-Ha Kim ◽  
Jisung Hwang ◽  
Ji Hoon Jung ◽  
Hyo-Jung Lee ◽  
Dae Young Lee ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Progression ◽  
Noncoding Rnas ◽  
Treg Cells ◽  
Molecular Networks ◽  
Cellular Immunotherapy ◽  
Clinical Implications ◽  
Immune Disorders ◽  
Dual Roles ◽  
Forkhead Box

AbstractThough Forkhead box P (FOXP) transcription factors comprising of FOXP1, FOXP2, FOXP3 and FOXP4 are involved in the embryonic development, immune disorders and cancer progression, the underlying function of FOXP3 targeting CD4 + CD25+ regulatory T (Treg) cells and the dual roles of FOXP proteins as an oncogene or a tumor suppressor are unclear and controversial in cancers to date. Thus, the present review highlighted research history, dual roles of FOXP proteins as a tumor suppressor or an oncogene, their molecular networks with other proteins and noncoding RNAs, cellular immunotherapy targeting FOXP3, and clinical implications in cancer progression.

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