Targeting MEX3A attenuates metastasis of breast cancer via β-catenin signaling pathway inhibition

Wang, Yun; Liang, Qian; Lei, Kefeng; Zhu, Qingqing; Zeng, Delong; Liu, Yuhong; Lu, Yingsi; Kang, Tingting; Tang, Nannan; Huang, Lifen; Ye, Liping; Tang, Di; Zhu, Chengming

doi:10.1016/j.canlet.2021.08.022

Cited by 13 publications

(9 citation statements)

References 40 publications

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“…MEX3A has been previously proved to promote the progression of breast cancer and other cancers [ 13 , 14 ]. Bioinformatics analysis revealed that MEX3A expression was evidently higher in CRC tissues than in normal tissues ( Figure 1a ).…”

Section: Resultsmentioning

confidence: 99%

MEX3A promotes angiogenesis in colorectal cancer via glycolysis

Zhou

et al. 2023

Libyan Journal of Medicine

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As a gastrointestinal malignancy, colorectal cancer (CRC) is a main cause of cancer-related deaths worldwide. Mex-3 RNA-binding family member A (MEX3A) is upregulated in multiple types of tumors and plays a critical role in tumor proliferation and metastasis. However, the function of MEX3A in CRC angiogenesis has not been fully understood. Hence, the aim of this study was to explore the role of MEX3A in CRC angiogenesis and investigate its underlying mechanisms. MEX3A expression in CRC was first investigated by bioinformatics means and then measured by qRT-PCR and Western blot. CCK-8 assay was employed to test cell viability. Angiogenesis assay was used to assess angiogenesis. The protein levels of VEGF, FGF and SDF-1 were evaluated using Western blot. The expression levels of MYC, HK2 and PGK1 were investigated by qRT-PCR. Extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were determined by Seahorse XP 96. The levels of pyruvate, lactate, citric acid and malate were measured by corresponding kits. Bioinformatics analysis demonstrated high MEX3A expression in CRC tissues and MEX3A enrichment in glycolysis and angiogenesis pathways. Cell assays showed high MEX3A expression in CRC cells and its promoting effects in CRC cell proliferation and glycolysis as well as angiogenesis. Rescue experiment confirmed that glycolysis inhibitor 2-DG could offset the promoting effects of MEX3A on the proliferation, angiogenesis and glycolysis of CRC cells. In conclusion, MEX3A could facilitate CRC angiogenesis by activating the glycolytic pathway, suggesting that MEX3A may be a novel therapeutic target for CRC.

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Section: Resultsmentioning

confidence: 99%

MEX3A promotes angiogenesis in colorectal cancer via glycolysis

Zhou

et al. 2023

Libyan Journal of Medicine

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“…For example, the luciferase reporter assay confirmed that the overexpression of B cell translocation gene 2, a target gene of the enhancer (chr1:203305170-203305671), might inhibit proliferation, invasion, and induce apoptosis in breast cancer cells. 46 , 47 The results of in vitro and in vivo studies showed that knockdown of MEX3A, a target gene of enhancers (chr1:156241956–156242457 and chr1:156051355-156051856), inhibited the metastasis and impaired the stemness of breast cancer cells. 28 , 47 The breast tissue microarray analysis confirmed that enhancer (chr8:123182900-123183401) target gene FAM83A is a potential biomarker for breast cancer initiation.…”

Section: Discussionmentioning

confidence: 99%

Identification of somatic mutation-driven enhancers and their clinical utility in breast cancer

Zhao,

Feng,

Lei

et al. 2024

iScience

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“…After 3 weeks, mice were sacri ced and xenograft tumors were harvested for histological study. The tumor volume was calculated according to the formula: Volume (mm 3 ) = width 2 (mm 2 ) × length (mm) × 0.4 [20] .…”

Section: Subcutaneous Xenograft Implantation Models and In Vivo Limit...mentioning

confidence: 99%

RANKL/RANK signaling recruits Tregs via CCL20/CCR6 pathway and promotes stemness and metastasis in colorectal cancers

Zhu,

Ouyang,

et al. 2024

Preprint

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TNF receptor superfamily member 11a (TNFRSF11a, RANK) and its ligand TNF superfamily member 11 (TNFRSF11, RANKL) are overexpressed in a number of malignancies. The clinical importance of RANKL/RANK in colorectal cancer (CRC) is, however, mainly unknown. We examined CRC patient samples and found that RANKL/RANK was elevated in CRC tissues as compared to nearby normal tissues. A higher RANKL/RANK expression was related with a worse survival rate. Furthermore, we found that RANKL is mostly produced by regulatory T cells (Tregs), which can promote CRC advancement. Overexpression of RANK or addition of RANKL significantly increased the stemness and migration of CRC cells. Furthermore, RANKL/RANK signaling stimulates C-C motif chemokine ligand 20 (CCL20) production by CRC cells, which leads to Treg recruitment, boosting tumor stemness and malignant progression. This recruitment process was accomplished by using CCL20-CCR6 interaction, demonstrating a connection between CRC cells and immune cells. These findings suggest that RANKL/RANK plays an important role in CRC progression and could be a potential target for CRC prevention and therapy.

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Targeting MEX3A attenuates metastasis of breast cancer via β-catenin signaling pathway inhibition

Cited by 13 publications

References 40 publications

MEX3A promotes angiogenesis in colorectal cancer via glycolysis

MEX3A promotes angiogenesis in colorectal cancer via glycolysis

Identification of somatic mutation-driven enhancers and their clinical utility in breast cancer

RANKL/RANK signaling recruits Tregs via CCL20/CCR6 pathway and promotes stemness and metastasis in colorectal cancers

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