MicroRNA-367 Inhibits Breast Cancer and Promotes Apoptosis by Targeting AT-Rich Interactive Domain-Containing Protein 1B

2022 ◽  
Vol 12 (4) ◽  
pp. 717-723
Author(s):  
Bing Pan ◽  
Binghui Liu ◽  
Juhua Pan ◽  
Jian Xin ◽  
Chenglin Fu
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Progression ◽  
Target Gene ◽  
Epithelial Tissue ◽  
Breast Epithelium ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Important Player ◽  
Epithelium Cells

Introduction: Breast cancer (BC) developed in the glandular epithelial tissue of breast. microRNA (miR)-367 is an important player in cancer progression, but has never been studied in BC. This experiment tries to probe the mechanism of miR-367 in BC treatment with downstream target gene. Materials and Methods: Human BC cell lines and healthy breast epithelium cells were applied in this study. After the transfection of miR-367 inhibitor or mimic into BC cells, functional assays were conducted to measure cell growth. Afterwards, flow cytometry was employed in apoptosis verification. Then, target relation between miR-367 and ARID1B was certified. Furthermore, ARID1B level was also measured. Results: miR-367 was underexpressed in human BC cells (p < 0.05). Besides, overexpressed miR-367 inhibited BC cell proliferation and encouraged apoptosis, while underexpressed miR-367 led to an opposite outcome (p < 0.05). This experiment then implied that miR-367 dramatically suppressed the activity of cell transfected with ARID1B-wild type. miR-367 overexpression quenched ARID1B level in BC cells; while silencing miR-367 upregulated ARID1B expression (p < 0.05). Conclusion: Our experiment discovered that miR-367 quenched BC cell growth and promoted apoptosis by targeting ARID1B. This investigation may provide novel insights in BC treatment.

scholarly journals LncRNA GAS5 Suppresses Ovarian Cancer Progression by Targeting miR-96-5p/PTEN Axis

2020 ◽  
Author(s):  
Qian Dong ◽  
Xiaoran Long ◽  
Jie Cheng ◽  
Xia Yin ◽  
Wenjing Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Progression ◽  
Target Gene ◽  
Growth Arrest ◽  
Mtor Signaling Pathway ◽  
Downstream Target ◽  
Specific Transcript ◽  
Downstream Target Gene ◽  
Non Coding Rnas ◽  
Proliferation And Invasion

Abstract Background Long non-coding RNAs (lncRNA) play critical roles in tumor occurrence and progression, including ovarian cancer (OC). The lncRNA growth arrest-specific transcript 5 (GAS5) has been proved to be an important modulator in the growth and metastasis of OC cells. Our studies confirm that GAS5 is down-regulated in OC; however, the potential molecular mechanism underlying it remains to be elucidated. Results In our study, we demonstrated that the expression levels of GAS5 and PTEN decreased, while miR-96-5p was up-regulated in ovarian cancer samples and cell lines compared with controls. PTEN is the downstream target gene of miR-96-5p. The up-regulation of GAS5 inhibited the expression of miR-96-5p, which directly targets PTEN. GAS5 overexpression can significantly reduce OC cell proliferation and invasion ability via suppression of miR-96-5p expression. PTEN/AKT/mTOR expression had a positive correlation with GAS5 expression. Moreover, miR-96-5p promoted OC progression by mediating PTEN/AKT/mTOR signaling pathway. Conclusion Our study identified GAS5 as a ceRNA which regulates the PTEN/AKT/mTOR axis through sponging miR-96-5p in OC.

scholarly journals Up-regulation of long non-coding RNA SNHG20 promotes ovarian cancer progression via Wnt/β-catenin signaling

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Shanyang He ◽  
Yunhe Zhao ◽  
Xiaoping Wang ◽  
Yalan Deng ◽  
Zhiyong Wan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Progression ◽  
Target Gene ◽  
Biological Function ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Downstream Target Gene ◽  
Long Non Coding Rna ◽  
Nucleolar Rna ◽  
Signaling Activity

Long non-coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to play crucial regulatory roles in many types of cancer. However, the biological function of long ncRNA (lncRNA) SNHG20 in ovarian cancer is still unclear. In the present study, we found that lncRNA SNHG20 was significantly increased in ovarian cancer. In addition, lncRNA SNHG20 knockdown suppressed the ovarian cancer progression, whereas overexpression of SNHG20 showed the opposite effects. Moreover, our results also revealed that lncRNA SNHG20 knockdown inhibited Wnt/β-catenin signaling activity by suppressing β-catenin expression and reversing the downstream target gene expression. Taken together, lncRNA SNHG20 plays an pivotal role in ovarian cancer progression by regulating Wnt/β-catenin signaling.

scholarly journals Long non-coding RNA MAFG-AS1 promotes proliferation and metastasis of breast cancer by modulating STC2 pathway

2020 ◽  
Author(s):  
Shihao Di ◽  
Die Lu ◽  
Chunni Chen ◽  
Tianshi Ma ◽  
Zigui Zou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Target Gene ◽  
Invasion And Metastasis ◽  
Cancer Proliferation ◽  
Downstream Target ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Downstream Target Gene ◽  
Proliferation And Metastasis ◽  
Long Non Coding Rna

Abstract Objective Breast cancer is the most common cancer in Chinese women. A number of studies proposed that long non-coding RNA plays an essential role in the regulation of invasion and metastasis of various forms of malignancy, including lung cancer, gastric cancer and bladder cancer. In this study, a long non-coding RNA MAFG-AS1 was explored in detail to understand the significance in the etiology of breast cancer.Methods Quantitative reverse transcription PCR (qRT-PCR) was used to examine the expression level of LncRNA MAFG-AS1 in tissues and cell lines. The association of LncRNA MAFG-AS1 expression and the postoperative prognosis was analyzed by the Kaplan-Meier method and log-rank test. Cell proliferation was evaluated in vitro and in vivo . Transwell assays were performed to examine the cell migration. Cell cycle and apoptosis was evaluated by flowcytometry analysis. The downstream target gene STC2 of LncRNA MAFG-AS1 was screened using the microarray analysis, which was validated by qRT-PCR, functional analysis, and rescue experiment.Results Expression of LncRNA MAFG-AS1 in the breast cancer tissues was significantly higher than the precancerous lesions. Elevated expression level of LncRNA MAFG-AS1 was correlated to the larger GTV (gross tumor volume), negative expression of ER, PR, Her2, lymph node metastasis, and poor prognosis. The potency of breast cancer proliferation, invasion and metastasis was inhibited in the absence of LncRNA MAFG-AS1.Tumorigenic capacity of breast cancer cells was inhibited in the absence of LncRNA MAFG-AS1. The downstream target gene regulated by LncRNA MAFG-AS1 was screened out by gene chip technology, GO analysis and QRT-PCR ultimately. Disrupted STC2 suppressed the cell proliferation and metastasis when the level of LncRNA MAFG-AS1 elevated.Conclusion The LncRNA MAFG-AS1 triggers tumorigenesis in the breast cancer and regulates breast cancer proliferation and metastasis by modulating the downstream target gene STC2. Results from our study indicates that LncRNA MAFG-AS1 can be used.

scholarly journals Fatty acid β-oxidation promotes breast cancer stemness and metastasis via the miRNA-328-3p-CPT1A pathway

2021 ◽  
Author(s):  
Feng Zeng ◽  
Mingkang Yao ◽  
Yun Wang ◽  
Wei Zheng ◽  
Shengshan Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fatty Acid ◽  
Target Gene ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Breast Cancer Patients ◽  
Potential Therapeutic Target ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Breast Cancer Growth

AbstractMicroRNAs (miRNA) have been shown to be associated with tumor diagnosis, prognosis, and therapeutic response. MiR-328-3p plays a significant role in breast cancer growth; however, its actual function and how it modulates specific biological functions is poorly understood. Here, miR-328-3p was significantly downregulated in breast cancer, especially in patients with metastasis. Mitochondrial carnitine palmitoyl transferase 1a (CPT1A) is a downstream target gene in the miR-328-3p-regulated pathway. Furthermore, the miR-328-3p/CPT1A/fatty acid β-oxidation/stemness axis was shown responsible for breast cancer metastasis. Collectively, this study revealed that miR-328-3p is a potential therapeutic target for the treatment of breast cancer patients with metastasis, and also a model for the miRNA-fatty acid β-oxidation-stemness axis, which may assist inunderstanding the cancer stem cell signaling functions of miRNA.

scholarly journals PRMT5-mediated methylation of YBX1 regulates NF-κB activity in colorectal cancer

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Antja-Voy Hartley ◽  
Benlian Wang ◽  
Rasika Mundade ◽  
Guanglong Jiang ◽  
Mengyao Sun ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Target Gene ◽  
Nuclear Factor Κb ◽  
Binding Ability ◽  
Multifunctional Protein ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Oncogenic Driver ◽  
First Time

Abstract The multifunctional protein Y-box binding protein 1 (YBX1), is a critical regulator of transcription and translation, and is widely recognized as an oncogenic driver in several solid tumors, including colorectal cancer (CRC). However, very little is known about the upstream or downstream factors that underlie YBX1′s regulation and involvement in CRC. Previously, we demonstrated that YBX1 overexpression correlated with potent activation of nuclear factor κB (NF-κB), a well-known transcription factor believed to be crucial in CRC progression. Here, we report a novel interaction between NF-κB, YBX1 and protein arginine methyltransferase 5 (PRMT5). Our findings reveal for the first time that PRMT5 catalyzes methylation of YBX1 at arginine 205 (YBX1-R205me2), an event that is critical for YBX1-mediated NF-κB activation and its downstream target gene expression. Importantly, when WT-YBX1 is overexpressed, this methylation exists under basal (unstimulated) conditions and is further augmented upon interleukin-1β (IL-1β) stimulation. Mechanistically, co-immunoprecipitation studies reveal that the R205 to alanine (A) mutant of YBX1 (YBX1-R205A) interacted less well with the p65 subunit of NF-κB and attenuated the DNA binding ability of p65. Importantly, overexpression of YBX1-R205A significantly reduced cell growth, migration and anchorage-independent growth of CRC cells. Collectively, our findings shed important light on the regulation of a novel PRMT5/YBX1/NF-κB axis through PRMT5-mediated YBX1-R205 methylation. Given the fact that PRMT5, YBX1 and NF-κB are all among top crucial factors in cancer progression, pharmacological disruption of this pivotal axis could serve as the basis for new therapeutics for CRC and other PRMT5/YBX1/NF-κB-associated cancers.

The Regulation of Downstream Target Gene AP-2γ by Transcription Factor OCT-4

2013 ◽  
Vol 40 (1) ◽  
pp. 43
Author(s):  
Xiao-Meng ZHAO ◽  
Cheng WANG ◽  
Xiao-Feng LI ◽  
Xiao-Ting ZHANG ◽  
Xi-Zhi LIU ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Target Gene ◽  
Downstream Target ◽  
Downstream Target Gene

Aryl Hydrocarbon Receptor: Its Regulation and Roles in Transformation and Tumorigenesis

2019 ◽  
Vol 20 (6) ◽  
pp. 625-634 ◽  
Author(s):  
Xun Che ◽  
Wei Dai
Keyword(s):  
Target Gene ◽  
Tumor Development ◽  
Environmental Response ◽  
Carcinogenic Effect ◽  
Post Translational Modifications ◽  
Downstream Target ◽  
Aryl Hydrocarbon ◽  
Downstream Target Gene ◽  
Major Mediator

AhR is an environmental response gene that mediates cellular responses to a variety of xenobiotic compounds that frequently function as AhR ligands. Many AhR ligands are classified as carcinogens or pro-carcinogens. Thus, AhR itself acts as a major mediator of the carcinogenic effect of many xenobiotics in vivo. In this concise review, mechanisms by which AhR trans-activates downstream target gene expression, modulates immune responses, and mediates malignant transformation and tumor development are discussed. Moreover, activation of AhR by post-translational modifications and crosstalk with other transcription factors or signaling pathways are also summarized.

Abstract 355: Exercise Prevents Doxorubicin-induced Cardiotoxicity via Targeting Microrna-669a-5p in Mice

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Yihua Bei ◽  
Jiahong Xu ◽  
Tianzhao Xu ◽  
Ping Chen ◽  
Lin Che ◽  
...  
Keyword(s):  
Protective Effect ◽  
Target Gene ◽  
Contractile Function ◽  
Cardiac Contractile Function ◽  
Downstream Target ◽  
Cardiac Contractile ◽  
Downstream Target Gene ◽  
Cardiac Ejection Fraction ◽  
Response To Exercise ◽  
Fractional Shortening

Doxorubicin (Dox)-induced cardiotoxicity, usually associated with increased oxidative stress, myofibrillar deterioration, and impaired cardiac contractile function, is a serious complication of antitumor therapy which may not be detected for many years. Growing evidence indicates that the regulation of cardiac microRNA (miRNA, miR) in response to exercise is essentially involved in the protective effect of exercise in the treatment of cardiovascular diseases. However, it is largely unknown whether and how exercise could prevent Dox-induced cardiotoxicity via regulating miRNA biology. In the current study, C57BL/6 mice were either subjected to a 3-week swimming program or remained sedentary. Mice were then treated with Dox (ip. 4 mg/kg/week for 4 weeks) to induce cardiotoxicity. Our data demonstrated that Dox resulted in marked reduction of cardiac ejection fraction (EF, %) and fractional shortening (FS, %) as measured by echocardiography. Interestingly, exercise significantly improved cardiac EF (%) and FS (%) in Dox-treated mice, indicating the protective effect of exercise in Dox-induced cardiotoxicity. Then, we performed microarray analysis (Affymetrix 3.0) showing that miR-27a-5p, miR-34b-3p, miR-185-3p, miR-203-3p, miR-669a-5p, miR-872-3p, and let-7i-3p were significantly reduced, while miR-2137 was increased in the hearts of exercised Dox-treated mice versus sedentary Dox-treated mice (FC(abs)>1.5, p<0.05). Using qRT-PCR, we further verified that miR-669a-5p was reduced by exercise training in Dox-treated mice. These data reveal that miR-669a-5p might be a potential miRNA mimicking the benefit of exercise in Dox-induced cardiotoxicity. Further study is needed to clarify the functional effect of miR-669a-5p and to identify its downstream target gene that contributes to the prevention and treatment of Dox-induced cardiotoxicity.

Regulation of a dpp target gene in the Drosophila embryo

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 303-311 ◽  
Author(s):  
J. Rusch ◽  
M. Levine
Keyword(s):  
Target Gene ◽  
Fusion Gene ◽  
Drosophila Embryo ◽  
Specific Expression ◽  
Downstream Target ◽  
Embryonic Tissues ◽  
Posterior Midgut ◽  
Downstream Target Gene ◽  
Genetic Epistasis ◽  
Vp16 Fusion

In Drosophila, two TGF-beta growth factors, dpp and screw, function synergistically to subdivide the dorsal ectoderm into two embryonic tissues, the amnioserosa and dorsal epidermis. Previous studies have shown that peak dpp activity is required for the localized expression of zerknullt (zen), which encodes a homeodomain transcription factor. We present evidence that zen directly activates the amnioserosa-specific expression of a downstream target gene, Race (Related to angiotensin converting enzyme). A 533 bp enhancer from the Race promoter region is shown to mediate selective expression in the amnioserosa, as well as the anterior and posterior midgut rudiments. This enhancer contains three zen protein binding sites, and mutations in these sites virtually abolish the expression of an otherwise normal Race-lacZ fusion gene in the amnioserosa, but not in the gut. Genetic epistasis experiments suggest that zen is not the sole activator of Race, although a hyperactivated form of zen (a zen-VP16 fusion protein) can partially complement reduced levels of dpp activity. These results suggest that dpp regulates multiple transcription factors, which function synergistically to specify the amnioserosa.

scholarly journals MicroRNA-346 inhibits the growth of glioma by directly targeting NFIB

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yangyang Li ◽  
Jia Xu ◽  
Jiale Zhang ◽  
Jie Zhang ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Target Gene ◽  
Glioma Cells ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
Direct Target ◽  
Proliferation Assays ◽  
The Relationship ◽  
Proliferation In Vitro

Abstract Background Glioma is considered one of the most common tumors and has a poor prognosis. Recently, microRNAs (miRNAs) have been reported to be strongly linked to various human tumors including glioma. In this study, we investigated a new anticancer miRNA, miR-346, to determine the effects and mechanism of miR-346 and its downstream target gene NFIB on tumors. Methods Lentivirus transfection, real-time PCR, western blotting, immunohistochemistry, cell proliferation assays, and mouse experiments were used to examine the relationship between miR-346 and its regulation of NFIB in glioma cells. Results The expression of miR-346 was downregulated in glioma cells. Overexpression of miR-346 arrested the cell cycle of glioma cells and inhibited their proliferation in vitro and in vivo. NFIB was a direct target of miR-346, whose expression was reduced by the miRNA. Overexpression of NFIB reversed all tested functions of miR-346. Conclusion miR-346 inhibited the growth of glioma cells by targeting NFIB and may be a new prognostic and diagnostic biomarker for glioma.

Sign in / Sign up

Export Citation Format

Share Document