CD133 expression is not selective for tumor-initiating or radioresistant cell populations in the CRC cell lines HCT-116

Dittfeld, Claudia; Dietrich, Antje; Peickert, Susann; Hering, Sandra; Baumann, Michaël; Grade, Marian; Ried, Thomas; Kunz-Schughart, Leoni A.

doi:10.1016/j.radonc.2009.06.034

Cited by 47 publications

(30 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because others questioned the validity of CD133 as a SLCCs marker [12], we incorporated another reported marker, CD44 [13,14], to further define SLCCs in HCT116 cells. We examined the expression of CD133 and CD44 in HCT116 cells by flow cytometry.…”

Section: Resultsmentioning

confidence: 99%

“…And CD133 ? cells were found not to be radioresistant in HCT116 colon cancer cells [12]. These data challenged the view that CD133 was an effective marker of colon SLCCs.…”

Section: Introductionmentioning

confidence: 90%

“…subset was enriched with tumorigenic capacity Previous reports showed confounding data regarding tumorigeneicity of CD133 ? cells in colon cancers [11,12]. We hypothesized that additional marker such as CD44 could better enrich tumorigenic capacity.…”

Section: Cd133-pementioning

confidence: 99%

See 2 more Smart Citations

Highly enriched CD133+CD44+ stem-like cells with CD133+CD44high metastatic subset in HCT116 colon cancer cells

Chen

Pan

Jiang

et al. 2011

Clin Exp Metastasis

View full text Add to dashboard Cite

Stem-like cancer cells (SLCCs) are distinct cellular subpopulation in colon cancer that is essential for tumor maintenance. Previous studies indicated that SLCCs accounted for only a minor subset in a given cancer model. However, we found that SLCCs frequency varied among a panel of colon cancer cell lines, with HCT116 cells composed mainly of SLCCs, as demonstrated by colonosphere forming capability and CD133 expression. Indeed, flow cytometric analysis revealed more than 60% HCT116 cells co-expressed the putative SLCCs markers CD133 and CD44. Compared with non-CD133(+)CD44(+) cells, FACS sorted CD133(+)CD44(+) cells were undifferentiated, endowed with extensive self-renewal and epithelial lineage differentiation capacity in vitro. CD133(+)CD44(+) exhibited enhanced tumorigeneicity in NOD/SCID mice. One thousand CD133(+)CD44(+) cells initiated xenograft tumors efficiently (3/6) while 1 × 10(5) non-CD133(+)CD44(+) cells could only form palpable nodule with much slower growth rate (1/6). More interestingly, long-term cultured self-renewing CD133(+)CD44(+) cells enriched CD133(+)CD44(high) subset, which expressed epithelial to mesenchymal transition marker, were more invasive in vitro and responsible solely for liver metastasis in vivo. In conclusion, these data demonstrated for the first time that CD133(+)CD44(+) SLCCs were highly enriched in HCT116 cells and that metastatic SLCCs resided exclusively in a CD133(+)CD44(high) subpopulation.

show abstract

Section: Resultsmentioning

confidence: 99%

“…And CD133 ? cells were found not to be radioresistant in HCT116 colon cancer cells [12]. These data challenged the view that CD133 was an effective marker of colon SLCCs.…”

Section: Introductionmentioning

confidence: 90%

See 1 more Smart Citation

Highly enriched CD133+CD44+ stem-like cells with CD133+CD44high metastatic subset in HCT116 colon cancer cells

Chen

Pan

Jiang

et al. 2011

Clin Exp Metastasis

View full text Add to dashboard Cite

show abstract

“…However, the validity of surface protein CD133 as a CSC marker was questioned [12,13,41]. Besides CD133, CD44, CD24, CD166 and ESA have been used individually or in combination for isolation and enrichment of colon CSCs [6][7][8]15,42].…”

Section: Discussionmentioning

confidence: 99%

“…However, Shmelkov et al [12] argued that expression patterns of CD133 were ubiquitous in differentiated epithelial cells and were not restricted to the CSC fraction in metastatic colon cancers. Further, CD133 + HCT116 colon cancer cells were found not to be radio resistant [13]. These data challenged the view that CD133 was an effective marker of colon CSCs.…”

Section: Introductionmentioning

confidence: 95%

Enrichment and Selective Targeting of Cancer Stem Cells in Colorectal Cancer Cell Lines

Wang¹,

Kanojia²,

Lo³

et al. 2013

Human Genet Embryol

View full text Add to dashboard Cite

Cancer stem cells (CSCs) are the subpopulation of cells within a tumor proposed to be responsible for tumor initiation, relapses, and resistance to chemotherapeutic drugs. Here we optimized sphere culture conditions to isolate and enrich CSCs from colorectal cancer cell line IMCE-Ras. Spheroid cells that developed in culture expressed high levels of putative stem cell markers, and showed stronger anchorage-independent growth abilities and resistance to conventional chemotherapeutic drugs compared with the initial monolayer adherent cells. Xenograft transplantation assays further demonstrated that IMCE-Ras spheroid cells are highly enriched in CSCs. To develop CSC-targeted therapy, we found that the relative percentage of CSC in IMCE-Ras cells was significantly decreased after a short duration exposure to DNA Methylation inhibitor 5-aza-2'-deoxycytidine (5-Aza-dC), indicating that DNA Methylation may be critical for self-renewal and maintenance of CSCs. Indeed, double knockout of DNA methyltransferase 1 (DNMT1) and DNA methyltransferase 3b (DNMT3b) in colon cancer cell line HCT116 resulted in loss of >95% DNA Methylation and complete loss of tumorigenicity both in vitro and in vivo. These data suggest that DNA Methylation is critical for maintenance of the colon CSC population, and a combination of classical chemotherapeutic drugs and DNA Methylation inhibitors may be an effective treatment of colon cancer.

show abstract

Do selective estrogen receptor modulators treat cervical precancer and cancer? Time to pool data from relevant trials

Castle¹

2010

Intl Journal of Cancer

View full text Add to dashboard Cite

Dear Editor,Based on the nearly absolute etiologic link between carcinogenic human papillomavirus (HPV) and cervical cancer, two new approaches for the prevention of cervical cancer have emerged: (1) HPV vaccination for primary HPV prevention in younger women and (2) carcinogenic HPV detection for secondary prevention via identifying and treating cervical precancer and early cancers. Both have demonstrated high degrees of efficacy with maximum effectiveness guided by an understanding of the causal model and application of these technologies in an age appropriate manner. 1 Despite the advent of these promising prevention tools, there is a real need to develop nonsurgical methods for treating cervical precancerous lesions and even early cancer for three reasons. First, current HPV vaccines are prophylactic and do not treat pre-existing HPV infections. 1 Second, surgical excision of screen-detected precancerous lesions, while a highly efficacious (90-95%) treatment 1 increases the risk of preterm delivery and infant morbidity and mortality. 2 Third, most women who screen positive by a Pap and/or HPV do not have clinically actionable disease, yet these women are at risk of cervical precancer and cancer in the future and must be followed up intensively. In addition, in the low-resource settings, surgical methods are not commonly available and cryotherapy, while moderately efficacious when its use is limited to smaller lesions, causes significant watery discharge and requires sexual abstinence for several weeks to permit healing of treated epithelium.Despite the knowledge that HPV infection is the obligate cause of cervical cancer, targeted immunological approaches for therapy such as therapeutic vaccines have been unsuccessful. 3 Chung and Lambert 4 present a novel approach of using estrogen receptor antagonists (selective estrogen receptor modulators or SERMs) to treat cervical precancer and cancer. As noted by the authors, there are strongly supportive laboratory 5 and epidemiological data 6,7 that estrogen plays contributing role in cervical carcinogenesis. In this study, Chung and Lambert 4 successfully treated 7 E6/E7 transgenic mice that spontaneously manifested cervical cancer with Raloxifene, an estrogen receptor antagonist that reduces the risk of breast cancer.To investigate whether Raloxifene might reduce the incidence of cervical cancer and its immediate precursor, carcinoma in situ (CIS), previously unpublished data on these outcomes from two randomized clinical trials to evaluate two SERMs, tamoxifen and raloxifene, for breast cancer risk reduction were analyzed. The NSABP (National Surgical Adjuvant Breast and Bowel Project), an NCI funded Cooperative Group, has designed and conducted the two large breast cancer prevention trials, Breast Cancer Prevention Trial P-1 (BCPT-P1) 8 and Study of Tamoxifen vs. Raloxifene (STAR). 9 While both tamoxifen and raloxifene are estrogen receptor antagonists in breast tissue, raloxifene is an estrogen receptor antagonist whereas tamoxifen is an agonist in the huma...

show abstract

CD133 expression is not selective for tumor-initiating or radioresistant cell populations in the CRC cell lines HCT-116

Cited by 47 publications

References 65 publications

Highly enriched CD133+CD44+ stem-like cells with CD133+CD44high metastatic subset in HCT116 colon cancer cells

Highly enriched CD133+CD44+ stem-like cells with CD133+CD44high metastatic subset in HCT116 colon cancer cells

Enrichment and Selective Targeting of Cancer Stem Cells in Colorectal Cancer Cell Lines

Do selective estrogen receptor modulators treat cervical precancer and cancer? Time to pool data from relevant trials

Contact Info

Product

Resources

About