CD51 correlates with the TGF-beta pathway and is a functional marker for colorectal cancer stem cells

Wang, J; Zhang, B; Wu, Haoxiang; Cai, Junchao; Sui, Xin; Wang, Y; Li, H; Qiu, Yuan; Wang, T; Chen, Z; Zhu, Qing; Xia, Hong-Fei; Wu, Song; Xiang, Andy Peng

doi:10.1038/onc.2016.299

Cited by 37 publications

(25 citation statements)

References 66 publications

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“…CD51, also known as integrin alpha-V, is reported to be expressed in nestin + colorectal cancer stem cells. 30 CD51 was also used to isolate nestin + mesenchymal stem cell (MSCs) in human fetal bone marrow. 31 However, CD51 cannot be used to identify adult nestin + MSCs, as both osteoblasts 32 and megakaryocytes 33 express CD51 in human adult marrow.…”

Section: Discussionmentioning

confidence: 99%

Transplanted human p75-positive stem Leydig cells replace disrupted Leydig cells for testosterone production

et al. 2017

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Previous studies have demonstrated that rodent stem Leydig cell (SLC) transplantation can partially restore testosterone production in Leydig cell (LC)-disrupted or senescent animal models, which provides a promising approach for the treatment of hypogonadism. Here, we isolated human SLCs prospectively and explored the potential therapeutic benefits of human SLC transplantation for hypogonadism treatment. In adult human testes, p75 neurotrophin receptor positive (p75+) cells expressed the known SLC marker nestin, but not the LC lineage marker hydroxysteroid dehydrogenase-3β (HSD3β). The p75+ cells which were sorted by flow cytometry from human adult testes could expand in vitro and exhibited clonogenic self-renewal capacity. The p75+ cells had multi-lineage differentiation potential into multiple mesodermal cell lineages and testosterone-producing LCs in vitro. After transplantation into the testes of ethane dimethane sulfonate (EDS)-treated LC-disrupted rat models, the p75+ cells differentiated into LCs in vivo and secreted testosterone in a physiological pattern. Moreover, p75+ cell transplantation accelerated the recovery of serum testosterone levels, spermatogenesis and reproductive organ weights. Taken together, we reported a method for the identification and isolation of human SLCs on the basis of p75 expression, and demonstrated that transplanted human p75+ SLCs could replace disrupted LCs for testosterone production. These findings provide the groundwork for further clinical application of human SLCs for hypogonadism.

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Section: Discussionmentioning

confidence: 99%

Transplanted human p75-positive stem Leydig cells replace disrupted Leydig cells for testosterone production

et al. 2017

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“…CSCs and EMT processes interact at molecular levels [ 70 ]. CSC marker CD51 is co-localized with type I TGF-β receptor (TβRI) and type II TGF-β receptor (TβRII) and enhances the TGF-β dependent accumulation of p-Smad2/3 in the nucleus, which upregulates EMT-related genes, such as PAI1, MMP9 and Snail, and promotes sphere formation, cell motility and tumor formation [ 26 ]. Therefore, it is speculated that metastasis of colorectal cancer is due to the EMT of colorectal CSCs, leading to loss of epithelial characteristics and acquisition of mesenchymal phenotypes.…”

Section: Colorectal Cscs In Progression Of Colorectal Cancermentioning

confidence: 99%

Cancer stem cells in progression of colorectal cancer

et al. 2017

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Colorectal cancer is one of the most common cancers worldwide with high mortality. Distant metastasis and relapse are major causes of patient death. Cancer stem cells (CSCs) play a critical role in the metastasis and relapse of colorectal cancer. CSCs are a subpopulation of cancer cells with unique properties of self-renewal, infinite division and multi-directional differentiation potential. Colorectal CSCs are defined with a group of cell surface markers, such as CD44, CD133, CD24, EpCAM, LGR5 and ALDH. They are highly tumorigenic, chemoresistant and radioresistant and thus are critical in the metastasis and recurrence of colorectal cancer and disease-free survival. This review article updates the colorectal CSCs with a focus on their role in tumor initiation, progression, drug resistance and tumor relapse.

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“…Next, we wished to test whether resveratrol and 5-FU treatments inhibited cancer stem cell-like phenotype in colon cancer cells. For HCT116, CD51 is a novel biomarker for colon cancer stemness [ 36 ]. We treated HCT116 cells with resveratrol alone and in combination with 5-FU, stained with CD51-Fitc antibody and applied to the flow cytometric analyses.…”

Section: Resultsmentioning

confidence: 99%

Combination of resveratrol and 5-flurouracil enhanced anti-telomerase activity and apoptosis by inhibiting STAT3 and Akt signaling pathways in human colorectal cancer cells

et al. 2018

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Colorectal cancer is one of the leading causes for mortalities worldwide. The most common cause of colorectal cancer mortality is hepatic metastasis. There has been a limited advancement in the targeted-therapies for metastatic colorectal cancer. Conventional chemotherapeutic agent 5-fluorouracil has been used for various cancer treatments including colorectal cancer. Development of drug resistance and severe toxicity are major hurdles for its use in clinical setting. Resveratrol is a natural polyphenolic compound which has protective effects against aging-related diseases. In this study, we have tested whether combined treatments of resveratrol and 5-FU enhanced inhibitory effects against colorectal cancer cell growth. We herein showed that resveratrol and 5-FU combination treatments caused the anti-cancer activities by simultaneously inhibiting STAT3 and Akt signaling pathways. Resveratrol treatment induced S-phase specific cell cycle arrest, and when combined with 5-FU, it showed further increase in colorectal cancer cell apoptosis. Combined treatments of resveratrol and 5-FU inhibited epithelial-mesenchymal transition. Notably, resveratrol showed anti-inflammatory effects by downregulating inflammatory biomarkers, pSTAT3 and pNFκB. Resveratrol and 5-FU treatments inhibited STAT3 phosphorylation and its binding to the promoter region of human telomerase reverse transcriptase (hTERT). Our data provide the first evidence that resveratrol can enhance anti-telomeric and pro-apoptotic potentials of 5-FU in colorectal cancer, hence lead to re-sensitization to chemotherapy.

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CD51 correlates with the TGF-beta pathway and is a functional marker for colorectal cancer stem cells

Cited by 37 publications

References 66 publications

Transplanted human p75-positive stem Leydig cells replace disrupted Leydig cells for testosterone production

Transplanted human p75-positive stem Leydig cells replace disrupted Leydig cells for testosterone production

Cancer stem cells in progression of colorectal cancer

Combination of resveratrol and 5-flurouracil enhanced anti-telomerase activity and apoptosis by inhibiting STAT3 and Akt signaling pathways in human colorectal cancer cells

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