scholarly journals Long Noncoding RNA HCG18 Promotes Malignant Phenotypes of Breast Cancer Cells via the HCG18/miR-103a-3p/UBE2O/mTORC1/HIF-1α–Positive Feedback Loop

2021 ◽  
Vol 9 ◽  
Author(s):  
Xu Liu ◽  
Kun Qiao ◽  
Kaiyuan Zhu ◽  
Xianglan Li ◽  
Chunbo Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Positive Feedback ◽  
Noncoding Rna ◽  
Feedback Loop ◽  
Hypoxia Inducible Factor ◽  
The Cancer Genome Atlas ◽  
Positive Feedback Loop ◽  
Downstream Target

In recent years, an increasing number of studies have reported that long noncoding RNAs (lncRNAs) play crucial roles in breast cancer (BC) progression and metastasis. Another study group of our research center reported that lncRNA HCG18 was one of the 30 upregulated lncRNAs in BC tissues compared with normal tissues in The Cancer Genome Atlas database. However, the exact biological roles of HCG18 in BC remain unclear. In this study, we demonstrated that HCG18 is significantly upregulated in BC tissues and cells and that BC patients with high HCG18 expression tend to have poor prognosis. In vitro assays indicated that HCG18 promotes BC cell proliferation and invasion and endows BC cells with cancer stemness properties. In vivo assays revealed that reducing HCG18 expression in the BC cell line MDA-MB-231 markedly decreased tumor growth and lung metastasis in xenograft mouse models. In terms of mechanism, we found that HCG18 positively regulated the expression of BC-related ubiquitin-conjugating enzyme E2O (UBE2O) by sponging miR-103a-3p, and our previous research verified that UBE2O could promote the malignant phenotypes of BC cells through the UBE2O/AMPKα2/mTORC1 axis. Furthermore, as a downstream target of the HCG18/miR-103a-3p/UBE2O/mTORC1 axis, hypoxia-inducible factor 1α transcriptionally promoted HCG18 expression and then formed a positive feedback loop in BC. Taken together, these results confirm that HCG18 plays an oncogenic role in BC and might serve as a prognostic biomarker and a potential therapeutic target for BC treatment.

Long non-coding RNA HCG18 promotes malignant phenotypes of breast cancer (BC) cells by HCG18/miR-103a-3p/UBE2O/mTORC1/HIF-1α positive feedback loop

2021 ◽  
Author(s):  
Xu Liu ◽  
Kun Qiao ◽  
Kaiyuan Zhu ◽  
Xianglan Li ◽  
Chunbo Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Luciferase Reporter ◽  
Regulatory Relationship ◽  
Positive Feedback Loop

Abstract Background: In recent years, a growing number of studies have reported that long non-coding RNAs (LncRNAs) play crucial roles in breast cancer (BC) progression and metastasis. Another study group of our research center reported that LncRNA HCG18 was one of the 30 upregulated lncRNAs in BC tissues related to normal tissues in TCGA database. However, the exactly biological roles of HCG18 in BC remains unclear. Method: qRT-PCR was used to detect the expression profile of HCG18 in BC tissues and cell lines. In vitro assays were used to evaluate the pro-tumor function of HCG18 in BC cells. Animal study were used to explore the role of HCG18 in vivo. Bioinformatic analysis, dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and Chromatin Immunoprecipitation (ChIP) assays were used to investigate the regulatory relationship of HCG18, miR-103a-3p, UBE2O in BC. Results: HCG18 was upregulated in BC tissues and cells, and BC patients with high HCG18 expression tended to have poor prognosis. HCG18 could promote BC cells proliferation, invasion and provided BC cells with tumor stemness properties (CSPs) in vitro and facilitate tumor growth and lung metastasis in vivo. In terms of mechanism, HCG18 functioned as a miRNA sponge which positively regulated the expression of Ubiquitin-conjugating enzyme E2O (UBE2O) by sponging miR-103a-3p and our previous research achievement have already verified UBE2O could promote malignant phenotypes of BC cells through UBE2O/AMPKα2/mTORC1 axis. Furthermore, as a downstream target of HCG18/miR-103a-3p/UBE2O/mTORC1 axis, HIF-1α transcriptionally promoted HCG18 expression and then formed a positive feedback loop in BC. Conclusion: HCG18 played an oncogenic role in BC and it might serve as a prognostic biomarker and a potential therapeutic target for BC treatment.

scholarly journals A Positive Feedback Loop of Long Noncoding RNA LINC00152 and KLF5 Facilitates Breast Cancer Growth

2021 ◽  
Vol 11 ◽  
Author(s):  
Qiang Li ◽  
Xiao Wang ◽  
Liheng Zhou ◽  
Mingyun Jiang ◽  
Guansheng Zhong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Positive Feedback ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Feedback Loop ◽  
Clinical Value ◽  
Survival Prognosis ◽  
Aberrant Expression ◽  
Positive Feedback Loop

The long noncoding RNA (lncRNA) LINC00152, also known as CYTOR, displays aberrant expression in various cancers. However, its clinical value and functional mechanisms in breast cancer remain insufficiently understood. Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis. Further studies revealed that LINC00152 knockdown suppresses cell proliferation and tumorigenicity in vitro and in vivo. Mechanistic analyses demonstrated that LINC00152 directly binds to KLF5 protein and increases KLF5 stability. Moreover, LINC00152 is also a KLF5-responsive lncRNA, and KLF5 activates LINC00152 transcription by directly binding to its promoter. Our study suggests that LINC00152 promotes tumor progression by interacting with KLF5. LINC00152 may be a valuable prognostic predictor for breast cancer, and the positive feedback loop of LINC00152-KLF5 could be a therapeutic target in pharmacological strategies.

scholarly journals CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 contributes to prostate carcinogenesis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Jin-Chun Qi ◽  
Zhan Yang ◽  
Tao Lin ◽  
Long Ma ◽  
Ya-Xuan Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcriptional Activation ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Biological Effects ◽  
Therapeutic Benefit ◽  
Loss Of Function ◽  
Positive Feedback Loop

Abstract Background Both E2F transcription factor and cyclin-dependent kinases (CDKs), which increase or decrease E2F activity by phosphorylating E2F or its partner, are involved in the control of cell proliferation, and some circRNAs and miRNAs regulate the expression of E2F and CDKs. However, little is known about whether dysregulation among E2Fs, CDKs, circRNAs and miRNAs occurs in human PCa. Methods The expression levels of CDK13 in PCa tissues and different cell lines were determined by quantitative real-time PCR and Western blot analysis. In vitro and in vivo assays were preformed to explore the biological effects of CDK13 in PCa cells. Co-immunoprecipitation anlysis coupled with mass spectrometry was used to identify E2F5 interaction with CDK13. A CRISPR-Cas9 complex was used to activate endogenous CDK13 and circCDK13 expression. Furthermore, the mechanism of circCDK13 was investigated by using loss-of-function and gain-of-function assays in vitro and in vivo. Results Here we show that CDK13 is significantly upregulated in human PCa tissues. CDK13 depletion and overexpression in PCa cells decrease and increase, respectively, cell proliferation, and the pro-proliferation effect of CDK13 is strengthened by its interaction with E2F5. Mechanistically, transcriptional activation of endogenous CDK13, but not the forced expression of CDK13 by its expression vector, remarkably promotes E2F5 protein expression by facilitating circCDK13 formation. Further, the upregulation of E2F5 enhances CDK13 transcription and promotes circCDK13 biogenesis, which in turn sponges miR-212-5p/449a and thus relieves their repression of the E2F5 expression, subsequently leading to the upregulation of E2F5 expression and PCa cell proliferation. Conclusions These findings suggest that CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 is responsible for PCa development. Targeting this newly identified regulatory axis may provide therapeutic benefit against PCa progression and drug resistance.

scholarly journals Interaction of Apoptotic Cells with Macrophages Upregulates COX-2/PGE2and HGF Expression via a Positive Feedback Loop

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Ji Yeon Byun ◽  
Young-So Youn ◽  
Ye-Ji Lee ◽  
Youn-Hee Choi ◽  
So-Yeon Woo ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Tissue Repair ◽  
Feedback Loop ◽  
Apoptotic Cell ◽  
Raw 264.7 Cells ◽  
Apoptotic Cells ◽  
Positive Feedback Loop ◽  
Cox 2

Recognition of apoptotic cells by macrophages is crucial for resolution of inflammation, immune tolerance, and tissue repair. Cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and hepatocyte growth factor (HGF) play important roles in the tissue repair process. We investigated the characteristics of macrophage COX-2 and PGE2expression mediated by apoptotic cells and then determined how macrophages exposed to apoptotic cellsin vitroandin vivoorchestrate the interaction between COX-2/PGE2and HGF signaling pathways. Exposure of RAW 264.7 cells and primary peritoneal macrophages to apoptotic cells resulted in induction of COX-2 and PGE2. The COX-2 inhibitor NS-398 suppressed apoptotic cell-induced PGE2production. Both NS-398 and COX-2-siRNA, as well as the PGE2receptor EP2 antagonist, blocked HGF expression in response to apoptotic cells. In addition, the HGF receptor antagonist suppressed increases in COX-2 and PGE2induction. Thein vivorelevance of the interaction between the COX-2/PGE2and HGF pathways through a positive feedback loop was shown in cultured alveolar macrophages followingin vivoexposure of bleomycin-stimulated lungs to apoptotic cells. Our results demonstrate that upregulation of the COX-2/PGE2and HGF in macrophages following exposure to apoptotic cells represents a mechanism for mediating the anti-inflammatory and antifibrotic consequences of apoptotic cell recognition.

scholarly journals A Positive Feedback Loop of lncRNA MIR31HG-miR-361-3p -YY1 Accelerates Colorectal Cancer Progression Through Modulating Proliferation, Angiogenesis, and Glycolysis

2021 ◽  
Vol 11 ◽  
Author(s):  
Tao Guo ◽  
Defeng Liu ◽  
Shihao Peng ◽  
Meng Wang ◽  
Yangyang Li
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Luciferase Reporter ◽  
Loss Of Function ◽  
Positive Feedback Loop ◽  
Related Proteins

BackgroundColorectal cancer (CRC) is a common malignant tumor with high metastatic and recurrent rates. This study probes the effect and mechanism of long non-coding RNA MIR31HG on the progression of CRC cells.Materials and MethodsQuantitative real-time PCR (qRT-PCR) was used to analyze the expression of MIR31HG and miR-361-3p in CRC tissues and normal tissues. Gain- or loss-of-function assays were conducted to examine the roles of MIR31HG, miR-361-3p and YY1 transcription factor (YY1) in the CRC progression. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and colony formation experiment were conducted to test CRC cell proliferation. CRC cell invasion was determined by Transwell assay. The glucose detection kit and lactic acid detection kit were utilized to monitor the levels of glucose and lactate in CRC cells. The glycolysis level in CRC cells was examined by the glycolytic stress experiment. Western blot was performed to compare the expression of glycolysis-related proteins (PKM2, GLUT1 and HK2) and angiogenesis-related proteins (including VEGFA, ANGPT1, HIF1A and TIMP1) in HUVECs. The binding relationships between MIR31HG and miR-361-3p, miR-361-3p and YY1 were evaluated by the dual-luciferase reporter assay and RNA immunoprecipitation (RIP).ResultsMIR31HG was up-regulated in CRC tissues and was associated with poorer prognosis of CRC patients. The in-vitro and in-vivo experiments confirmed that overexpressing MIR31HG heightened the proliferation, growth, invasion, glycolysis and lung metastasis of CRC cells as well as the angiogenesis of HUVECs. In addition, MIR3HG overexpression promoted YY1 mRNA and protein level, and forced overexpression of YY1 enhanced MIR31HG level. Overexpressing YY1 reversed the tumor-suppressive effect mediated by MIR31HG knockdown. miR-361-3p, which was inhibited by MIR31HG overexpression, repressed the malignant behaviors of CRC cells. miR-361-3p-mediated anti-tumor effects were mostly reversed by upregulating MIR31HG. Further mechanism studies illustrated that miR-361-3p targeted and negatively regulated the expression of YY1.ConclusionThis study reveals that MIR31HG functions as an oncogenic gene in CRC via forming a positive feedback loop of MIR31HG-miR-361-3p-YY1.

scholarly journals Novel Long Noncoding RNA 005620 Induces Epirubicin Resistance in Triple-Negative Breast Cancer by Regulating ITGB1 Expression

2021 ◽  
Vol 11 ◽  
Author(s):  
Fengliang Wang ◽  
Sujin Yang ◽  
Mingming Lv ◽  
Fei Chen ◽  
Hong Yin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Noncoding Rna ◽  
Triple Negative ◽  
Sequencing Analysis ◽  
Loss Of Function ◽  
Integrin Β1 ◽  
Downstream Target

Triple-negative breast cancer (TNBC) is often treated with anthracyclines (e.g., epirubicin or doxorubicin), but very little is known about anthracycline resistance, especially epirubicin resistance in TNBC. To identify novel long noncoding RNAs (lncRNAs) involved in epirubicin resistance in TNBC, we established a new TNBC MDA-MB-231 cell line that was resistant to epirubicin (Epi-R). A total of 12 differentially expressed lncRNAs were identified using RNA sequencing analysis of Epi-R cells. Among these lncRNAs, we found a novel intronic lncRNA, lnc005620, was highly expressed in Epi-R cells and human TNBC tissues. Further gain- and loss-of-function studies demonstrated that lnc005620 played an oncogenic role and partially abrogated the effects of epirubicin on TNBC cells. Using iTRAQ proteomics analysis, we found that three members of the integrin family, integrin β4, integrin β1 and integrin α6, were all upregulated in Epi-R MDA-MB-231 cells. Integrin β1, encoded by the ITGB1 gene, was validated to be a downstream target of lnc005620 in Epi-R MDA-MB-231 cells. Our study demonstrates that novel lnc005620 promotes TNBC progression and chemoresistance to epirubicin via integrin β1 both in vitro and in vivo and provides a promising therapeutic target for TNBC patients in terms of enhancing the benefits of epirubicin treatment.

scholarly journals DNMT1-induced miR-378a-3p silencing promotes angiogenesis via the NF-κB signaling pathway by targeting TRAF1 in hepatocellular carcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Bin Zhu ◽  
Jun-Jie Chen ◽  
Ying Feng ◽  
Jun-Ling Yang ◽  
Hua Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Positive Feedback ◽  
Dna Methyltransferase ◽  
Feedback Loop ◽  
Tube Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Positive Feedback Loop

Abstract Background Angiogenesis plays an important role in the occurrence, development and metastasis of hepatocellular carcinoma (HCC). According to previous studies, miR-378a participates in tumorigenesis and tumor metastasis, but its exact role in HCC angiogenesis remains poorly understood. Methods qRT-PCR was used to investigate the expression of miR-378a-3p in HCC tissues and cell lines. The effects of miR-378a-3p on HCC in vitro and in vivo were examined by Cell Counting Kit-8 (CCK-8), Transwell, tube formation and Matrigel plug assays, RNA sequencing, bioinformatics, luciferase reporter, immunofluorescence and chromatin immunoprecipitation (ChIP) assays were used to detect the molecular mechanism by which miR-378a-3p inhibits angiogenesis. Results We confirmed that miR-378a-3p expression was significantly downregulated and associated with higher microvascular density (MVD) in HCC; miR-378a-3p downregulation indicated a short survival time in HCC patients. miR-378a-3p knockdown led to a significant increase in angiogenesis in vitro and in vivo. We found that miR-378a-3p directly targeted TNF receptor associated factor 1 (TRAF1) to attenuate NF-κB signaling, and then downregulated secreted vascular endothelial growth factor. DNA methyltransferase 1 (DNMT1)-mediated hypermethylation of miR-378a-3p was responsible for downregulating miR-378a-3p. Moreover, a series of investigations indicated that p65 initiated a positive feedback loop that could upregulate DNMT1 to promote hypermethylation of the miR-378a-3p promoter. Conclusion Our study indicates a novel DNMT1/miR-378a-3p/TRAF1/NF-κB positive feedback loop in HCC cells, which may become a potential therapeutic target for HCC.

scholarly journals ITGB1-DT Facilitates Lung Adenocarcinoma Progression via Forming a Positive Feedback Loop With ITGB1/Wnt/β-Catenin/MYC

2021 ◽  
Vol 9 ◽  
Author(s):  
Ruimin Chang ◽  
Xiaoxiong Xiao ◽  
Yao Fu ◽  
Chunfang Zhang ◽  
Xiaoyan Zhu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Cellular Proliferation ◽  
Disease Free Survival ◽  
Migration And Invasion ◽  
Poor Overall Survival ◽  
Positive Feedback Loop ◽  
Downstream Target

Lung adenocarcinoma (LUAD) is the main histological type of lung cancer, which is the leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) were recently revealed to be involved in various cancers. However, the clinical relevance and potential biological roles of most lncRNAs in LUAD remain unclear. Here, we identified a prognosis-related lncRNA ITGB1-DT in LUAD. ITGB1-DT was upregulated in LUAD and high expression of ITGB1-DT was correlated with advanced clinical stages and poor overall survival and disease-free survival. Enhanced expression of ITGB1-DT facilitated LUAD cellular proliferation, migration, and invasion, and also lung metastasis in vivo. Knockdown of ITGB1-DT repressed LUAD cellular proliferation, migration, and invasion. ITGB1-DT interacted with EZH2, repressed the binding of EZH2 to ITGB1 promoter, reduced H3K27me3 levels at ITGB1 promoter region, and therefore activated ITGB1 expression. Through upregulating ITGB1, ITGB1-DT activated Wnt/β-catenin pathway and its downstream target MYC in LUAD. The expressions of ITGB1-DT, ITGB1, and MYC were positively correlated with each other in LUAD tissues. Intriguingly, ITGB1-DT was found as a transcriptional target of MYC. MYC directly transcriptionally activated ITGB1-DT expression. Thus, ITGB1-DT formed a positive feedback loop with ITGB1/Wnt/β-catenin/MYC. The oncogenic roles of ITGB1-DT were reversed by depletion of ITGB1 or inhibition of Wnt/β-catenin pathway. In summary, these findings revealed ITGB1-DT as a prognosis-related and oncogenic lncRNA in LUAD via activating the ITGB1-DT/ITGB1/Wnt/β-catenin/MYC positive feedback loop. These results implicated ITGB1-DT as a potential prognostic biomarker and therapeutic target for LUAD.

scholarly journals C-MYC inducible onco-lncRNA LINC00036 acting as EGFR mRNA stabilizer via RNA-protein and RNA-RNA interactions decreases the sensitivity of gefitinib in human cancer

2021 ◽  
Author(s):  
Shouping Xu ◽  
Lin Wan ◽  
Qin Wang ◽  
Huizi Yin ◽  
Kun Qiao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Molecular Mechanism ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Human Cancer ◽  
Luciferase Reporter ◽  
Positive Feedback Loop ◽  
Different Types

Abstract Background: The oncogenic lncRNA based strategies for combating cancer may usher in a new and promising paradigm in cancer therapy. However, few studies have been performed to solve such a critical issue. The complex traits and molecular mechanism of such lncRNAs in tumorigenesis and their relationship with sensitivity of gefitinib in human cancer have not been investigated.Methods: We aimed to identify and validate such a novel oncogenic LINC00036 using transcriptome sequencing approach and a large number of tissue samples of different types of cancer from the our cancer center cohort and public data cohorts from the Cancer Genome Atlas，Gene Expression Omnibus and Cancer Cell Line Encyclopedia. Moreover, series of in vitro and in vivo experiments were performed to examine its roles in tumorigenesis and the sensitivity of gefitinib in different types of cancer cells. Special nanoparticle via a more potent delivery system was developed to investigate the feasibility of targeting LINC00036 in vivo. Furthermore, chromatin immunoprecipitation (ChIP)-sequencing, ChIP, actinomycin D assay, dual-luciferase reporter assay, RNA pull-down and RNA immunoprecipitation were performed were developed to uncover the molecular mechanism.Results: LINC00036 that associated with poor prognosis is significantly upregulated in human cancer tissues. Series of in vitro and in vivo experiments reveal that LINC00036 promotes tumorigenesis and decreases the sensitivity of gefitinib in different types of cancer cells. LINC00036 targeting nanoparticle markedly reduced the growth of human cancer xenografts. Mechanistically, LINC00036 is a direct transcriptional target of c-MYC and a positive feedback loop of the c-MYC-LINC00036-EGFR axis exists in human cancer. LINC00036 acts as an EGFR mRNA stabilizer via RNA-protein and RNA-RNA interactions, inducing the hyper-activation of the downstream AKT and MAPK signaling pathways, which in turn decreases the sensitivity of gefitinib in human cancer.Conclusions: LINC00036, a c-MYC inducible onco-lncRNA, acts an oncogene in human cancer and decreases the sensitivity of gefitinib through positive feedback loop of the c-MYC-LINC00036-EGFR axis. Overall, this study broadens knowledge regarding novel onco-lncRNAs and will assist in developing feasible onco-lncRNAs based-targeted therapeutic strategies to improve the sensitivity of gefitinib in human cancer.

scholarly journals UBE2O promotes the proliferation, EMT and stemness properties of breast cancer cells through the UBE2O/AMPKα2/mTORC1-MYC positive feedback loop

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Xu Liu ◽  
Fei Ma ◽  
Chunxiao Liu ◽  
Kaiyuan Zhu ◽  
Wenjie Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Positive Feedback ◽  
Feedback Loop ◽  
In Vitro Assays ◽  
Positive Feedback Loop ◽  
Ubiquitin Conjugating Enzyme ◽  
Mesenchymal Transformation ◽  
Conjugating Enzyme

AbstractUbiquitin-conjugating enzyme E2O (UBE2O) is a large E2 ubiquitin-conjugating enzyme that possesses both E2 and E3 ligase activities. Ectopic UBE2O overexpression is associated with a variety of human diseases, especially cancers. However, the expression profile and functional biology of UBE2O in human breast cancer (BC) remain unclear. In this study, we found that UBE2O was significantly overexpressed in human BC tissues and cells. Patients with high UBE2O expression tended to have a high risk of metastasis and poor prognosis. In vitro assays revealed that UBE2O promoted BC cell proliferation and epithelial–mesenchymal transformation (EMT) and endowed BC cells with cancer stemness properties (CSPs). UBE2O knockdown in MDA-MB-231 cells suppressed tumour growth and lung metastasis in MDA-MB-231 xenograft mouse models. Mechanistically, UBE2O functioned as a ubiquitin enzyme of AMPKα2, promoting its ubiquitination and degradation and thus activating the mTORC1 signal pathway and contributing to BC oncogenesis and metastasis. Furthermore, as a downstream factor of the UBE2O/AMPKα2/mTORC1 axis, the oncoprotein MYC transcriptionally promoted UBE2O and formed a positive feedback loop in human BC. Collectively, our study demonstrated that UBE2O/AMPKα2/mTORC1-MYC forms a positive feedback loop in human BC cells that regulates BC cell proliferation and EMT and endows BC cells with CSPs.

Sign in / Sign up

Export Citation Format

Share Document