The role of microRNA-4723-5p regulated by c-myc in triple-negative breast cancer

Jin, Xi-Xin; Gao, Chao; Wei, Wenxin; Chong, Jong‐Wha; Li, Li; Ma, Binlin; Dong, Chao

doi:10.1080/21655979.2022.2056824

Cited by 3 publications

(2 citation statements)

References 37 publications

(26 reference statements)

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“…Previous findings suggest that FUBP1 may play a role in the carcinogenesis process by relying on the c-Myc pathway [ 39 ]. Compared with the results of Jin et al [ 38 ]. This study further identified the important role of FUBP1 binding to c-Myc in colon cancer progression.…”

Section: Discussionmentioning

confidence: 60%

“…Moreover, Ding et al [ 19 ] found that c-Myc was expressed in more than 75% of gliomas, and its high expression was also related to the low survival rate of human gliomas. Jin et al showed that c-Myc knockout could inhibit the occurrence and metastasis of triple negative breast cancer by reducing the expression of Hsa-mir-4723-5p [ 38 ]. Treating c-Myc-dependent tumors could be achieved by affecting the expression of FUBP1 [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

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Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Wang

et al. 2022

Bioengineered

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Human distal upstream element (Fuse) binding protein 1 (FUBP1) is a transcriptional regulator of c-Myc and represents an important prognostic marker in many cancers. Therefore, the present study aimed to investigate whether FUBP1 could combine with c-Myc to participate in the progression of colon cancer. Detection of FUBP1 expression was done through reverse transcription-quantitative PCR (RT-qPCR), and the combination of FUBP1 and c-Myc was detected by immunoprecipitation assay. Cell counting kit (CCK)-8, colony formation, transwell and wound healing were applied for assessing the ability of cells to proliferate, migrate, and invade; glycolysis and lactic acid detection kits were used to detect glucose uptake and lactic acid content, while western blotting was adopted to detect the protein expression of glycolysis-related genes. FUBP1 expression was elevated in HCT116 cells relative to other colon cancer cell lines, and silencing FUBP1 could inhibit the ability of HCT116 cells to proliferate, migrate, invade and glycolysis, and enhance its apoptosis. In addition, the results of immunoprecipitation experiments showed that FUBP1 could bind to c-Myc. c-Myc overexpression reversed the inhibitory effects of FUBP1 knockdown on the ability of HCT116 cells to proliferate, migrate, invade and glycolysis. The results indicated that FUBP1 could participate in the deterioration process of colon cancer cells by combining with c-Myc, and it has clinical significance for understanding the key role of FUBP1 in tumor genesis.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Wang

et al. 2022

Bioengineered

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Stemness of Cancer: A Study of Triple-negative Breast Cancer From a Neuroscience Perspective

Djamgoz

2024

Stem Cell Rev and Rep

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Stemness, giving cancer cells massive plasticity enabling them to survive in dynamic (e.g. hypoxic) environments and become resistant to treatment, especially chemotherapy, is an important property of aggressive tumours. Here, we review some essentials of cancer stemness focusing on triple-negative breast cancer (TNBC), the most aggressive form of all breast cancers. TNBC cells express a range of genes and mechanisms associated with stemness, including the fundamental four “Yamanaka factors”. Most of the evidence concerns the transcription factor / oncogene c-Myc and an interesting case is the expression of the neonatal splice variant of voltage-gated sodium channel subtype Nav1.5. On the whole, measures that reduce the stemness make cancer cells less aggressive, reducing their invasive/metastatic potential and increasing/restoring their chemosensitivity. Such measures include gene silencing techniques, epigenetic therapies as well as novel approaches like optogenetics aiming to modulate the plasma membrane voltage. Indeed, simply hyperpolarizing their membrane potential can make stem cells differentiate. Finally, we give an overview of the clinical aspects and exploitation of cancer/TNBC stemness, including diagnostics and therapeutics. In particular, personalised mRNA-based therapies and mechanistically meaningful combinations are promising and the emerging discipline of ‘cancer neuroscience’ is providing novel insights to both fundamental issues and clinical applications. Graphical Abstract

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Role of Harmaline in Inhibiting c-Myc, Altering Molecular Typing, and Promoting Apoptosis in Triple-Negative Breast Cancer

Xu,

Ma,

et al. 2024

BCTT

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Objective Triple-negative breast cancer (TNBC) lacks effective targeted, endocrine therapeutic agents and the development of novel agents is costly and time-consuming. The objective of this study was to identify pharmaceuticals and natural products utilized in clinical practice that have the potential to inhibit the expression of Cellular-myelocytomatosis oncogene (c-Myc), based on a review of the current literature. The aim was to assess the effect of the specified drugs on c-Myc expression in TNBC cells, determine the most potent inhibitor, and evaluate its impact on TNBC cell proliferation, invasive migration, and apoptosis, as well as the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2) at both the gene and protein levels. Explore its potential for treatment or adjuvant therapy for triple-negative breast cancer. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to quantify gene and protein expression levels. Flow cytometry was employed to measure cell proliferation and apoptosis, while the Transwell assay was utilized to assess cell invasion and migration. Results Harmaline emerged as the strongest inhibitor, significantly decreasing the expression of c-Myc at both the gene and protein levels in TNBC cells. It also inhibited cell proliferation, invasion, and migration while promoting apoptosis in TNBC cells. Additionally, there was a varying increase in the expression of ER and PR genes and proteins. While the expression of the HER-2 gene was elevated, there was no significant change in HER-2 protein levels. Notably, the expression of the phosphorylated HER-2 protein increased. Conclusion Harmaline was found to promote apoptosis and inhibit cell proliferation, invasion, and migration in TNBC cells by targeting the inhibition of c-Myc. It also induced the re-expression of the ER, PR, and HER-2 genes, as well as the ER and PR proteins.

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The role of microRNA-4723-5p regulated by c-myc in triple-negative breast cancer

Cited by 3 publications

References 37 publications

Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc

Stemness of Cancer: A Study of Triple-negative Breast Cancer From a Neuroscience Perspective

Role of Harmaline in Inhibiting c-Myc, Altering Molecular Typing, and Promoting Apoptosis in Triple-Negative Breast Cancer

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