CD26 a cancer stem cell marker and therapeutic target

Davies, Samuel; Beckenkamp, Aline; Buffon, Andréia

doi:10.1016/j.biopha.2015.02.031

Cited by 41 publications

(40 citation statements)

References 35 publications

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“…Since our experiments have proved strong Warburg effect in the MtDP PC3 cells, the main CD44 + /Δψ m Low population in the MtDP PC3 cells are highly indicated to be Warburg effect and cell stemness-linked. In line with this assumption, our transcription profiling also confirmed upregulated expression of a series of other cancer stem cells related genes including Aldh1a , integrin α2β1 and Cd26 [29, 36, 61–64]. …”

Section: Discussionsupporting

confidence: 82%

MtDNA depleted PC3 cells exhibit Warburg effect and cancer stem cell features

Lü

et al. 2016

Oncotarget

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Reducing mtDNA content was considered as a critical step in the metabolism restructuring for cell stemness restoration and further neoplastic development. However, the connections between mtDNA depletion and metabolism reprograming-based cancer cell stemness in prostate cancers are still lack of studies. Here, we demonstrated that human CRPC cell line PC3 tolerated high concentration of the mtDNA replication inhibitor ethidium bromide (EtBr) and the mtDNA depletion triggered a universal metabolic remodeling process. Failure in completing that process caused lethal consequences. The mtDNA depleted (MtDP) PC3 cells could be steadily maintained in the special medium in slow cycling status. The MtDP PC3 cells contained immature mitochondria and exhibited Warburg effect. Furthermore, the MtDP PC3 cells were resistant to therapeutic treatments and contained greater cancer stem cell-like subpopulations: CD44+, ABCG2+, side-population and ALDHbright. In conclusion, these results highlight the association of mtDNA content, mitochondrial function and cancer cell stemness features.

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Section: Discussionsupporting

confidence: 82%

MtDNA depleted PC3 cells exhibit Warburg effect and cancer stem cell features

Lü

et al. 2016

Oncotarget

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“…Recent studies have determined that the biological functions of CD26 are related to metastatic capacity in colorectal CSCs, 10, 11 while CXCR4 is regarded as a key receptor that is closely involved in tumor invasion and metastasis. Therefore, we selected CD26 and CXCR4 as markers of invasive stemness 12, 13 and performed flow cytometry-based cell sorting on the cell spheroids based on the expression of CD26 and CXCR4. The CD26-positive cells and CXCR4-positive cells accounted for 2.59 and 0.929% of the gastric cancer cells, respectively, and the double-positive cells and double-negative cells accounted for 0.995 and 95.5% of the gastric cancer cells, respectively (Figure 2a).…”

Section: Resultsmentioning

confidence: 99%

The promotion of the transformation of quiescent gastric cancer stem cells by IL-17 and the underlying mechanisms

et al. 2016

Oncogene

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Postoperative recurrence and metastasis have crucial roles in the poor prognosis of gastric cancer patients. Previous studies have indicated that gastric cancer originates from cancer stem cells (CSCs), and some investigators have found that a particular subset of CSCs possesses higher metastatic capacity. However, the specific mechanism remains uncertain. In the present study, we aimed to explore the biological functions of the inflammatory cytokine interleukin-17 (IL-17) in gastric cancer metastasis and the distinct IL-17-induced transformation of quiescent gastric CSCs. Our results showed that invasive gastric CSCs were CD26+ and CXCR4+ and were closely associated with increased metastatic ability. The quiescent gastric CSCs, which were CD26 − and CXCR4 − , were exposed to appropriate concentrations of IL-17; this resulted in the decreased expression of E-cadherin and the increased expression of vimentin and N-cadherin. In addition, the upregulation of IL-17 both in vitro and in vivo resulted in a significant induction of invasion, migration and tumor formation ability in gastric CSCs compared with the control group, which was not treated with IL-17. Further experiments indicated that the activation of the downstream phosphorylated signal transducer and activator of transcription 3 (STAT3) transcription factor pathway was facilitated by IL-17. On the contrary, the downregulation of STAT3 by the specific inhibitor Stattic significantly reversed the IL-17-induced epithelial-mesenchymal transition (EMT)-associated properties of quiescent gastric CSCs. Moreover, tumorigenesis and metastasis were suppressed. Taken together, we suggest that IL-17 is positively correlated with the transformation of quiescent gastric CSCs into invasive gastric CSCs and that targeting IL-17 may emerge as a possible novel therapeutic strategy for gastric cancer. INTRODUCTIONGastric cancer is one of the most common gastrointestinal malignancies, and the morbidity and mortality of patients with gastric cancer remain high. Key biological characteristics of gastric cancer include invasion and metastasis, which are the main factors that are responsible for postoperative recurrence and the development of therapeutic resistance. Studies focused on the mechanisms that underlie the invasion and metastasis of gastric cancer have attracted extensive attention, but these mechanisms have not been fully elucidated. 1,2 An increasing amount of evidence supports the cancer stem cell (CSC) theory. This theory proposes that CSCs serve not only as the basis for the development and progression of tumors but also as the primary reason for tumor recurrence and metastasis. Recent studies have demonstrated that CSCs are heterogeneous. CSCs are divided into different subsets including quiescent CSCs and invasive CSCs based on their distinct characteristics. Invasive CSC is a major motivation to cancer metastasis. Additionally, quiescent CSCs may differentiate into invasive CSCs in specific microenvironments, thereby promoting distant tumor metastasis. 3,4 As ...

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“…DPPIV has been implicated in the initial stages of malignant transformation and tumor progression, as well as immune regulation [14, 16, 26]. However, DPPIV also reportedly acts as a tumor suppressor [20–23] or oncogene [18, 19, 27, 28], and this may depend on the characteristics of individual cell lines and tumors. Understanding the mechanisms underlying DPPIV activity may clarify these contradictory findings [29, 30].…”

Section: Discussionmentioning

confidence: 99%

DPPIV promotes endometrial carcinoma cell proliferation, invasion and tumorigenesis

Yang

Zhang

et al. 2017

Oncotarget

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Dipeptidyl peptidase IV (DPPIV), also known as CD26, is a 110-kDa cell surface glycoprotein expressed in various tissues. DPPIV reportedly plays a direct role in the progression of several human malignancies. DPPIV specific inhibitors are employed as antidiabetics and could potentially be repurposed to enhance anti-tumor immunotherapies. In the present study, we investigated the correlation between DPPIV expression and tumor progression in endometrial carcinoma (EC). DPPIV overexpression altered cell morphology and stimulated cell proliferation, invasion and tumorigenesis in vitro and in vivo. These effects were abrogated by DPPIV knockdown or pharmacological inhibition using sitagliptin. DPPIV overexpression increased hypoxia-inducible factor 1a (HIF-1a) and vascular endothelial growth factor A (VEGFA) expression to promote HIF-1a-VEGFA signaling. Our results indicated that DPPIV accelerated endometrial carcinoma progression and that sitagliptin may be an effective anti-EC therapeutic.

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CD26 a cancer stem cell marker and therapeutic target

Cited by 41 publications

References 35 publications

MtDNA depleted PC3 cells exhibit Warburg effect and cancer stem cell features

MtDNA depleted PC3 cells exhibit Warburg effect and cancer stem cell features

The promotion of the transformation of quiescent gastric cancer stem cells by IL-17 and the underlying mechanisms

DPPIV promotes endometrial carcinoma cell proliferation, invasion and tumorigenesis

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