Last update 01 Nov 2024

c-Myc x CD44

Last update 01 Nov 2024

Basic Info

Related Targets

c-MycCD44

Drugs associated with c-Myc x CD44

CircCDK13

Target

CD44 x c-Myc

Mechanism

CD44 modulators [+1]

Active Org.

Tianjin Medical University

Originator Org.

Tianjin Medical University

Active Indication

Diabetic ulcer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with c-Myc x CD44

100 Translational Medicine associated with c-Myc x CD44

0 Patents (Medical) associated with c-Myc x CD44

430

Literatures (Medical) associated with c-Myc x CD44

31 Dec 2024·Gut Microbes

Commensal microbiota-derived metabolite agmatine triggers inflammation to promote colorectal tumorigenesis

Article

Author: Zhang, Xiaobo ; Cui, Aoxi ; Lu, Yu

Colorectal cancer (CRC), a malignant tumor worldwide, is associated with gut microbiota. The influence of gut microbe-derived metabolites on CRC has attracted a lot of attention. However, the role of immunity mediated by commensal microbiota-derived metabolites in tumorigenesis of CRC is not intensively explored. Here we monitored the gut microbial dysbiosis in CRC mouse model (Apc^Min/+ model) without dietary and pharmacological intervention, followed by characterized of metabolites enriched in CRC model mice. Profound changes of gut microbiome (bacteriome) were observed during intestinal disorders. Metabolomic profiling indicated that agmatine, derived from the gut bacteria i.e. Blautia, Odoribacter, Alistipes and Paraprevotella, could interact with Rnf128 to suppress the Rnf128-mediated ubiquitination of β-catenin to further upregulate the downstream targets of β-catenin including Cyclin D1, Lgr5, CD44 and C-myc, thus activating Wnt signaling. The activated Wnt signaling pathway promoted dysplasia of intestinal cells and inflammatory infiltration of lymphocytes via inducing the upregulation of pro-inflammatory cytokines (IL-6 and TNF-α) and downregulation of anti-inflammatory cytokine (IL-10), thereby contributing to colorectal carcinogenesis. Therefore, our study presented novel insights into the roles and mechanisms of gut microbiota in pathogenesis of CRC.

01 Dec 2024·Cellular and Molecular Life Sciences

WNT5A regulates the proliferation, apoptosis and stemness of human stem Leydig cells via the β-catenin signaling pathway

Article

Author: He, Caimei ; Liu, Wei ; He, Zuping ; Cui, Yinghong ; Du, Li

Stem Leydig cells (SLCs) are essential for maintaining normal spermatogenesis as the significant component of testis microenvironment and gonadal aging. Although progress has been achieved in the regulation of male germ cells in mammals and humans, it remains unknown about the genes and signaling pathways of human SLCs. Here we have demonstrated, for the first time, that WNT5A (Wnt family member 5a) mediates the proliferation, apoptosis, and stemness of human SLCs, namely NGFR⁺ Leydig cells. We revealed that NGFR⁺ Leydig cells expressed NGFR, PDGFRA, NES, NR2F2, and THY1, hallmarks for SLCs. RNA-sequencing showed that WNT5A was expressed at a higher level in human SLCs than non-SLCs, while immunohistochemistry and Western blots further illustrated that WNT5A was predominantly expressed in human SLCs. Notably, CCK-8, EdU and Western blots displayed that WNT5A enhanced the proliferation and DNA synthesis and retained stemness of human SLCs, whereas flow cytometry and TUNEL analyses demonstrated that WNT5A inhibited the apoptosis of these cells. WNT5A knockdown caused an increase in LC lineage differentiation of human SLCs and reversed the effect of WNT5A overexpression on fate decisions of human SLCs. In addition, WNT5A silencing resulted in the decreases in nuclear translocation of β-catenin and expression levels of c-Myc, CD44, and Cyclin D1. Collectively, these results implicate that WNT5A regulates the proliferation, apoptosis and stemness of human SLCs through the activation of the β-catenin signaling pathway. This study thus provides a novel molecular mechanism underlying the fate determinations of human SLCs, and it offers a new insight into the niche regulation of human testis.

01 Dec 2024·Molecular Biology Reports

Effects of CD44 siRNA on inhibition, survival, and apoptosis of breast cancer cell lines (MDA-MB-231 and 4T1)

Article

Author: Baradaran, Behzad ; Moghaddamneshat, Nilofar ; Dehbokri, Shaho Ghahremani ; Noorolyai, Saeed ; Baghbani, Elham ; Javaheri, Tohid

BACKGROUNDBreast cancer (BC) is one of the most common cancers in the world. Despite the many advances that have been made in treating patients, many patients are still resistant to treatment. CD44 is one of the surface glycoproteins of BC cells that plays an important role in the proliferation of these cells and inhibition of their apoptosis. Therefore, targeting it can be a treatment way for BC patients.METHODSIn this study, the effect of anti-CD44 siRNA on the proliferation, apoptosis, and migration rate of MDA-MB-231 and 4T1 cells was investigated. The techniques used in this study were MTT assay, RT-PCR, and flow cytometry.RESULTSThe apoptosis and proliferation rates in CD44 siRNA-treated cells were higher and lower, respectively, compared to untreated cells. Also, cell migration was less in treated cells compared to untreated cells. CD44 siRNA also decreased the expression of CXCR4, c-myc, Vimentin, ROCK, and MMP-9.CONCLUSIONFinally, CD44 targeting can be a good treatment option to make BC cells more sensitive to apoptosis.

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