High CD133 Expression in the Nucleus and Cytoplasm Predicts Poor Prognosis in Non-Small Cell Lung Cancer

Huang, Minjie; Zhu, Huijun; Feng, Jian; Ni, Songshi; Huang, Jianfei

doi:10.1155/2015/986095

Cited by 36 publications

(40 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One surprising observation in our study is the translocation of full‐length Prom1 (as other proteins) into the nuclear compartment. This finding is nonetheless in line with publications describing the presence of Prom1 in the nucleus of cells, which might be an indicator of poor prognosis in cancer (Cantile et al , ; Huang et al , ). How can a plasma membrane protein reach the nucleoplasm?…”

Section: Discussionsupporting

confidence: 92%

Prominin‐1 controls stem cell activation by orchestrating ciliary dynamics

et al. 2018

View full text Add to dashboard Cite

Proper temporal and spatial activation of stem cells relies on highly coordinated cell signaling. The primary cilium is the sensory organelle that is responsible for transmitting extracellular signals into a cell. Primary cilium size, architecture, and assembly–disassembly dynamics are under rigid cell cycle‐dependent control. Using mouse incisor tooth epithelia as a model, we show that ciliary dynamics in stem cells require the proper functions of a cholesterol‐binding membrane glycoprotein, Prominin‐1 (Prom1/CD133), which controls sequential recruitment of ciliary membrane components, histone deacetylase, and transcription factors. Nuclear translocation of Prom1 and these molecules is particularly evident in transit amplifying cells, the immediate derivatives of stem cells. The absence of Prom1 impairs ciliary dynamics and abolishes the growth stimulation effects of sonic hedgehog (SHH) treatment, resulting in the disruption of stem cell quiescence maintenance and activation. We propose that Prom1 is a key regulator ensuring appropriate response of stem cells to extracellular signals, with important implications for development, regeneration, and diseases.

show abstract

Section: Discussionsupporting

confidence: 92%

Prominin‐1 controls stem cell activation by orchestrating ciliary dynamics

et al. 2018

View full text Add to dashboard Cite

show abstract

“…During our recent study aimed at the analysis of CSC markers in pediatric sarcomas, we noted a surprising result: a stable subset of cells in each of five RMS cell lines examined exhibited an exclusive nuclear localization of CD133 (these data are published in this article). To date, a similar localization of this antigen has been described only in one case report of breast cancer ( 14 ) and in a large study on lung cancer ( 15 ) using immunohistochemical methods, nevertheless, without any verification or systematic description. For this reason, in this study, we sought to analyze this interesting phenomenon in detail using three independent anti-CD133 commercial antibodies ( Fig.…”

Section: Introductionmentioning

confidence: 94%

Atypical nuclear localization of CD133 plasma membrane glycoprotein in rhabdomyosarcoma cell lines

Nunukova

Neradil

Škoda

et al. 2015

International Journal of Molecular Medicine

View full text Add to dashboard Cite

CD133 (also known as prominin-1) is a cell surface glycoprotein that is widely used for the identification of stem cells. Furthermore, its glycosylated epitope, AC133, has recently been discussed as a marker of cancer stem cells in various human malignancies. During our recent experiments on rhabdomyosarcomas (RMS), we unexpectedly identified an atypical nuclear localization of CD133 in a relatively stable subset of cells in five RMS cell lines established in our laboratory. To the best of our knowledge, this atypical localization of CD133 has not yet been proven or analyzed in detail in cancer cells. In the present study, we verified the nuclear localization of CD133 in RMS cells using three independent anti-CD133 antibodies, including both rabbit polyclonal and mouse monoclonal antibodies. Indirect immunofluorescence and confocal microscopy followed by software cross-section analysis, transmission electron microscopy and cell fractionation with immunoblotting were also employed, and all the results undeniably confirmed the presence of CD133 in the nuclei of stable minor subpopulations of all five RMS cell lines. The proportion of cells showing an exclusive nuclear localization of CD133 ranged from 3.4 to 7.5%, with only minor differences observed among the individual anti-CD133 antibodies. Although the role of CD133 in the cell nucleus remains unclear, these results clearly indicate that this atypical nuclear localization of CD133 in a minor subpopulation of cancer cells is a common phenomenon in RMS cell lines.

show abstract

“…Stem cells group harboring in tissues of patients with NSCLC were detected by using markers of either ALDH1 or CD133, as were reported and applied before. [28][29][30][31][32][33][34][35] Higher ratios of both ALDH1C cells ( Fig. 1A) and CD133C (Fig.…”

Section: Ratios Of Cancer Stem Cells In Nsclc Correlates With Prognosismentioning

confidence: 99%

miR-367 stimulates Wnt cascade activation through degrading FBXW7 in NSCLC stem cells

Xiao

Zhang

et al. 2017

Cell Cycle

View full text Add to dashboard Cite

Lung carcinoma tops the categories of cancer related motility, and has been treated as the main threat to human health. The functions and related mechanism of FBXW7 controlled lung cancer stem cells' signatures is barely unknown, and the miR-367 regulations of FBXW7 via Wnt signaling have not been explored. Cancer stem cells of either ALDH1+ or CD133+ phenotype were found to be referred to advanced stages in patients with NSCLC (non-small cell lung carcinoma). To study the roles of miR-367, we found greater miR-367 level or FBXW7 level was reserved in NSCLC than that of paired adjacent normal tissues, and their upregulations were positively correlated with Wnt signaling activation. On the contrary, increased miR-367 was correlated with Let-7 repression. MiR-367 was related to stronger sphere forming ability in stem cells of NSCLC. We then explored the functions of the endogenous miR-367 in stem-like cells isolated from NSCLC cell lines. In HEK-293 cells, we identified FBXW7 as the direct downstream gene of miR-367, which consequently released the LIN-28 dependent inhibition of suppressive Let-7. Through informatics analysis, miR-367 was predicated to function through Wnt signaling, and decreased Let-7 played the pivotal role to maintain TCF-4/Wnt pathway activity. The reintroduction of FBXW7 abolished the oncogenic stimulation of miR-367 on TCF-4 activity, with Wnt signaling factors depression. In conclusion, our findings demonstrated the oncogenic roles of miR-367 exerting on the self-renewal ability of cancer stem-like cells through degrading the suppressive FBXW7, eventually helping to maintain Wnt signaling activation through a LIN28B/Let-7 dependent manner.

show abstract

High CD133 Expression in the Nucleus and Cytoplasm Predicts Poor Prognosis in Non-Small Cell Lung Cancer

Cited by 36 publications

References 42 publications

Prominin‐1 controls stem cell activation by orchestrating ciliary dynamics

Prominin‐1 controls stem cell activation by orchestrating ciliary dynamics

Atypical nuclear localization of CD133 plasma membrane glycoprotein in rhabdomyosarcoma cell lines

miR-367 stimulates Wnt cascade activation through degrading FBXW7 in NSCLC stem cells

Contact Info

Product

Resources

About