Cancer stem cell markers and their prognostic value

Mv, Puchinskaya

doi:10.17116/patol201678247-54

Cited by 8 publications

(5 citation statements)

References 65 publications

(105 reference statements)

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“…To elucidate the underlying mechanism of melatonin and its possibility of paclitaxel sensitizer, the current work was performed in X02 cancer stem cells. Herein CXCR4, CD44, CD133, CD90, SOX‐2, and nestin at protein level and nestin, A20, CXCR4 at mRNA level as stem cell markers were highly expressed in X02 cells compared to other cancer cells such as U87, U373, and T98G cells in X02 cells, indicating X02 cells have stem cell property. Furthermore, melatonin disturbed sphere formation and renewal property in a time‐dependent fashion as well as reduced the expression of SOX‐2, CXCR4, nestin, and NANOG in X02 cells, implying inhibitory effect of melatonin on cancer stem cell (CSC) property.…”

Section: Discussionmentioning

confidence: 88%

Melatonin disturbs SUMOylation‐mediated crosstalk between c‐Myc and nestin via MT1 activation and promotes the sensitivity of paclitaxel in brain cancer stem cells

Lee

Jung

Shin

et al. 2018

Journal of Pineal Research

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Here the underlying antitumor mechanism of melatonin and its potency as a sensitizer of paclitaxel was investigated in X02 cancer stem cells. Melatonin suppressed sphere formation and induced G2/M arrest in X02 cells expressing nestin, CD133, CXCR4, and SOX-2 as biomarkers of stemness. Furthermore, melatonin reduced the expression of CDK2, CDK4, cyclin D1, cyclin E, and c-Myc and upregulated cyclin B1 in X02 cells. Notably, genes of c-Myc related mRNAs were differentially expressed in melatonin-treated X02 cells by microarray analysis. Consistently, melatonin reduced the expression of c-Myc at mRNA and protein levels, which was blocked by MG132. Of note, overexpression of c-Myc increased the expression of nestin, while overexpression of nestin enhanced c-Myc through crosstalk despite different locations, nucleus, and cytoplasm. Interestingly, melatonin attenuated small ubiquitin-related modifier-1 (SUMO-1) more than SUMO-2 or SUMO-3 and disturbed nuclear translocation of nestin for direct binding to c-Myc by SUMOylation of SUMO-1 protein by immunofluorescence and immunoprecipitation. Also, melatonin reduced trimethylated histone H3K4me3 and H3K36me3 more than dimethylation in X02 cells by Western blotting and chromatin immunoprecipitation assay. Notably, melatonin upregulated MT1, not MT2, in X02 cells and melatonin receptor inhibitor luzindole blocked the ability of melatonin to decrease the expression of nestin, p-c-Myc(S62), and c-Myc. Furthermore, melatonin promoted cytotoxicity, sub-G1 accumulation, and apoptotic body formation by Paclitaxcel in X02 cells. Taken together, these findings suggest that melatonin inhibits stemness via suppression of c-Myc, nestin, and histone methylation via MT1 activation and promotes anticancer effect of Paclitaxcel in brain cancer stem cells.

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Section: Discussionmentioning

confidence: 88%

Melatonin disturbs SUMOylation‐mediated crosstalk between c‐Myc and nestin via MT1 activation and promotes the sensitivity of paclitaxel in brain cancer stem cells

Lee

Jung

Shin

et al. 2018

Journal of Pineal Research

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“…Therefore, novel CSC markers for SK-BR-3 cells are required. As leukocyte differentiation antigens have been used as stem cell markers in a number of tumors (28), this study investigated the alterations in leukocyte differentiation antigens, among which CD24, CD109 and CD164 exhibited increased expression in SK-BR-3 cells (Fig. 3A; Table II).…”

Section: Resultsmentioning

confidence: 99%

Identification of new cancer stem cell markers and signaling pathways in HER‑2‑positive breast cancer by transcriptome sequencing

Huang

et al. 2019

Int J Oncol

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Human epidermal growth factor receptor (HER)-2-positive breast cancer accounts for ~25% of all breast cancer cases, has a high propensity for relapse, metastasis and drug resistance, and is associated with a poor prognosis. Therefore, it is necessary to develop more effective therapeutic targets for the treatment of HER-2-positive breast cancer. CD44+/CD24−/low is currently the most commonly used marker for breast cancer stem cells (CSCs), which are considered the main cause of drug resistance, relapse and metastasis. In the present study, the ratio of CD44+/CD24−/low cells was almost zero in SK-BR-3 cells; however, it was >90% in MDA-MB-231 cells, as determined by flow cytometry. Since SK-BR-3 and MDA-MB-231 cells both exhibit a strong propensity for invasion and migration, it was hypothesized that there may be other markers of CSCs in SK-BR-3 cells. Therefore, transcriptome sequencing was performed for SK-BR-3 and MDA-MB-231 cells. It was observed that several leukocyte differentiation antigens and other CSC markers were significantly more highly expressed in SK-BR-3 cells. Furthermore, the expression of aldehyde dehydrogenase (ALDH)1A3, CD164 and epithelial cell adhesion molecule (EpCAM) was higher in SK-BR-3 cells compared with in other subtypes of breast cell lines, as determined by reverse transcription-polymerase chain reaction and western blot analysis. In addition, the expression levels of ALDH1A3, ALDH3B2 and EpCAM were higher in HER-2-positive breast cancer compared with in paracancerous tissues and other subtypes of breast cancer, as determined by immunohistochemistry. The expression of β-catenin in the Wnt signaling pathway was lower in SK-BR-3 cells compared with in MDA-MB-231 cells, which may be used as a prognostic indicator for breast cancer. These findings may help identify novel CSC markers and therapeutic targets for HER-2-positive breast cancer.

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“…Apoptosis can be triggered externally by specific transmembrane proteins-death receptors [85][86][87]. In addition, the formation of the apoptotic signal can be initiated by the binding of NPs to proteins that play a key role in tumor growth [88]. For example, superparamagnetic nanoparticles (NiFe and magnetite nanodisks) used in [89] and functionalized for binding to the renal carcinoma tumor membrane antigen (CA9 [90] carboanthidase) induced apoptosis 6 h after bioconjugate injection and exposure to a non-heating (≈30 mT) low-frequency (≈20 Hz) magnetic field.…”

Section: Scenarios Of the Malignant Cell Apoptosis And Related Proces...mentioning

confidence: 99%

Towards understanding the triggering of the malignant cell death in high-efficiency magneto-mechanical anticancer therapy

Semina¹,

Isaev²,

Комогорцев³

et al. 2023

J. Phys. D: Appl. Phys.

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The paper discusses schemes for the implementation of magneto-mechanical anticancer therapy and the most probable scenarios of damaging mechanical eﬀects on the membranes of malignant cells by targeted magnetic nanoparticles selectively bound to membrane mechanoreceptors employing aptamers. The conditions for selective triggering of the malignant cell apoptosis in a low-frequency non-heating alternating magnetic ﬁeld, corresponding to the exceeding threshold value of the force acting on the membrane and its mechanoreceptors, are established using a nanoparticle dynamic simulation. The requirements for the functionality of magnetic nanoparticles and their suitability for biomedical applications are analysed. Attention is paid to the possibility of the formation of magnetite nanoparticle aggregates in an external magnetic ﬁeld and their localization near tumor cell membranes. It is shown that the scenario involving the process of aggregation of magnetite nanoparticles provides a suﬃcient magneto-mechanical impact to achieve a therapeutic eﬀect. A possible explanation for the experimentally established fact of successful application of magneto-mechanical therapy using magnetite nanoparticles is presented, in which complete suppression of the Ehrlich carcinoma in an alternating magnetic ﬁeld as a response to a magnetome-chanical stimulus was demonstrated. This result conﬁrmed the possibility of using the method for high eﬃciency treatment of malignant neoplasms. The paper is provided with an extensive review of key publications and the state of art in this area.

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Cancer stem cell markers and their prognostic value

Cited by 8 publications

References 65 publications

Melatonin disturbs SUMOylation‐mediated crosstalk between c‐Myc and nestin via MT1 activation and promotes the sensitivity of paclitaxel in brain cancer stem cells

Melatonin disturbs SUMOylation‐mediated crosstalk between c‐Myc and nestin via MT1 activation and promotes the sensitivity of paclitaxel in brain cancer stem cells

Identification of new cancer stem cell markers and signaling pathways in HER‑2‑positive breast cancer by transcriptome sequencing

Towards understanding the triggering of the malignant cell death in high-efficiency magneto-mechanical anticancer therapy

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