Acquisition of tumorigenic potential and therapeutic resistance in CD133+ subpopulation of prostate cancer cells exhibiting stem-cell like characteristics

Kanwal, Rajnee; Shukla, Sanjeev; Walker, Ethan; Gupta, Sanjay

doi:10.1016/j.canlet.2018.05.014

Cited by 43 publications

(45 citation statements)

References 48 publications

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“…Previous works have demonstrated that XRCC1 is associated with tumor resistance to chemotherapy and radiotherapy, carcinogenesis, and tumor progression (Sak et al, 2005;Hanssen-Bauer et al, 2012;Xu et al, 2014;Li et al, 2018). CD133 + cancer cells are a small subgroup of tumor cells and related to tumor resistance to chemotherapy and radiotherapy (Zhang et al, 2010;Desai et al, 2014;Vincent et al, 2014;Kanwal et al, 2018). Thus, we further studied the clinicopathological and prognostic significance of XRCC1 in gallbladder SC/ASC and AC, and evaluated the biological role of XRCC1 in CD133 + GBC-SD cells.…”

Section: Discussionmentioning

confidence: 92%

XRCC1 Is a Promising Predictive Biomarker and Facilitates Chemo-Resistance in Gallbladder Cancer

Miao

et al. 2020

Front. Mol. Biosci.

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Gallbladder cancer is a relatively uncommon human malignant tumor with an extremely poor prognosis. Currently, no biomarkers can accurately diagnose gallbladder cancer and predict patients' prognosis. XRCC1 is involved in tumorigenesis, progression, and chemo-resistance of several human cancers, but the role of XRCC1 in gallbladder cancer is never reported. In this study, we investigated the expression of XRCC1 and its clinicopathological and prognostic significance in gallbladder cancer, and explored the biological role of XRCC1 in gallbladder cancer cells. We found that XRCC1 was significantly up-regulated in gallbladder cancer in protein and mRNA levels. Positive XRCC1 expression was correlated with aggressive clinicopathological features and was an independent poor prognostic factor in gallbladder cancer. The ROC curves suggested that XRCC1 expression had potential clinicopathological diagnostic value in gallbladder cancer. In vitro, XRCC1 was overexpression in CD133 + GBC-SD cells compared to GBC-SD cells. In functional experiment, XRCC1 knockdown had a non-significant impact on proliferation, migration, invasion, and apoptosis of CD133 + GBC-SD cells. But, XRCC1 knockdown could significantly improve the sensitivity of CD133 + GBC-SD cells to 5-Fluorouracil via promoting cell necrosis and apoptosis. Thus, this study indicates that XRCC1 may be a promising predictive biomarker of gallbladder cancer and a potential therapeutic target for gallbladder cancer.

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Section: Discussionmentioning

confidence: 92%

XRCC1 Is a Promising Predictive Biomarker and Facilitates Chemo-Resistance in Gallbladder Cancer

Miao

et al. 2020

Front. Mol. Biosci.

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“…To evaluate whether the neuroendocrine phenotype was linked to the induction of stemness properties and plasticity in prostate cancer, we determined the expression of the well-known stem markers CD133 and ALDH1A1. The pentaspan transmembrane glycoprotein CD133 is the most frequently used cell surface antigen to detect CSCs from various solid tumors including prostate tumors [21] and to isolate prostate stem cells from a population of primary human prostate cancer cell lines [22]. In addition, it is overexpressed in aggressive androgen-independent prostate cancer [23].…”

Section: Establishment Of Prostate Stem-like Cellsmentioning

confidence: 99%

Androgen Deprivation Induces Reprogramming of Prostate Cancer Cells to Stem-Like Cells

Sánchez

Vara-Ciruelos

Díaz‐Laviada

2020

Cells

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In the past few years, cell plasticity has emerged as a mode of targeted therapy evasion in prostate adenocarcinoma. When exposed to anticancer therapies, tumor cells may switch into a different histological subtype, such as the neuroendocrine phenotype which is associated with treatment failure and a poor prognosis. In this study, we demonstrated that long-term androgen signal depletion of prostate LNCaP cells induced a neuroendocrine phenotype followed by re-differentiation towards a “stem-like” state. LNCaP cells incubated for 30 days in charcoal-stripped medium or with the androgen receptor antagonist 2-hydroxyflutamide developed neuroendocrine morphology and increased the expression of the neuroendocrine markers βIII-tubulin and neuron specific enolase (NSE). When cells were incubated for 90 days in androgen-depleted medium, they grew as floating spheres and had enhanced expression of the stem cell markers CD133, ALDH1A1, and the transporter ABCB1A. Additionally, the pluripotent transcription factors Nanog and Oct4 and the angiogenic factor VEGF were up-regulated while the expression of E-cadherin was inhibited. Cell viability revealed that those cells were resistant to docetaxel and 2-hidroxyflutamide. Mechanistically, androgen depletion induced the decrease in AMP-activated kinase (AMPK) expression and activation and stabilization of the hypoxia-inducible factor HIF-1α. Overexpression of AMPK in the stem-like cells decreased the expression of stem markers as well as that of HIF-1α and VEGF while it restored the levels of E-cadherin and PGC-1α. Most importantly, docetaxel sensitivity was restored in stem-like AMPK-transfected cells. Our model provides a new regulatory mechanism of prostate cancer plasticity through AMPK that is worth exploring.

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“…This finding showed that a lack of Cygb results in an increase of the CD133 (+) LCSC subpopulation and LCSC phenotypes, whereas Cygb restoration ameliorates CD133 (+) LCSC subpopulation and LCSC phenotypes (Figure ). The CD133 (+) subpopulation of prostate cancer cells exhibits an increasing resistance to γ‐radiation and chemotherapeutic drugs . ALDH1 deregulation sensitizes lung cancer‐initiating cells to cisplatin .…”

Section: Discussionmentioning

confidence: 97%

“…The CD133 (+) subpopulation of prostate cancer cells exhibits an increasing resistance to γ-radiation and chemotherapeutic drugs. 36 ALDH1 deregulation sensitizes lung cancer-initiating cells to cisplatin. 37 Thus we proposed that Cygb could be a newly therapeutic target against LCSCs.…”

Section: Cscs Are a Crucial Subpopulation Of Cancer Cells Targetingmentioning

confidence: 99%

Cytoglobin ameliorates the stemness of hepatocellular carcinoma via coupling oxidative‐nitrosative stress signals

Zhang

Pei

Yang

et al. 2018

Molecular Carcinogenesis

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Cancer stem cells (CSCs) account for tumor self‐renewal and heterogeneity. Oxidative‐nitrosative stress (ONS) is an independent etiologic factor throughout tumorigenesis. Emerging evidences indicated that the interaction of ONS with CSCs contributes to tumor progression and resistance to chemoradiotherapy. Cytoglobin (Cygb) is a member of human hexacoordinate hemoglobin family and acts as a dynamic mediator of redox homeostasis. We observed that Cygb is significantly deregulated in human hepatocellular carcinoma (HCC) tissue and its decrease aggravates the growth of liver cancer stem cells (LCSCs) and increases the subpopulation of CD133(+) LCSCs. Cygb restoration inhibits HCC proliferation and LCSC growth, and decreases the subpopulation of CD133 (+) LCSCs in vitro. We found that Cygb absence promotes LCSC phenotypes and PI3 K/AKT activation, whereas Cygb restoration inhibits LCSC phenotypes and PI3 K/AKT activation. Furthermore, exogenous antioxidants can eliminate the inhibitory effect of Cygb to LCSC growth and phenotypes, as well as PI3 K/AKT activation. Collectively, this study demonstrated that cytoglobin functions as a tumor suppressor and targets CSCs at an ONS‐dependent manner. Thus, Cygb restoration could be a novel and promising therapeutic strategy against HCC with aberrant ROS/RNS accumulation.

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Acquisition of tumorigenic potential and therapeutic resistance in CD133+ subpopulation of prostate cancer cells exhibiting stem-cell like characteristics

Cited by 43 publications

References 48 publications

XRCC1 Is a Promising Predictive Biomarker and Facilitates Chemo-Resistance in Gallbladder Cancer

XRCC1 Is a Promising Predictive Biomarker and Facilitates Chemo-Resistance in Gallbladder Cancer

Androgen Deprivation Induces Reprogramming of Prostate Cancer Cells to Stem-Like Cells

Cytoglobin ameliorates the stemness of hepatocellular carcinoma via coupling oxidative‐nitrosative stress signals

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