Biological characteristics of a sub-population of cancer stem cells from two triple-negative breast tumour cell lines

Enciso-Benavides, Javier; Alfaro, Luis; Castañeda-Altamirano, Carlos; Rojas, Nancy; González-Cabeza, José; Enciso, Nathaly; Riesco, Fernando; Castillo, Miluska; Enciso, Javier

doi:10.1016/j.heliyon.2021.e07273

Cited by 14 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cancer stem cells have the ability to self-renew, differentiate, and initiate tumor growth and metastasis. The identification of markers that are specific to CSCs is important for understanding their biology and developing targeted therapies [ 4 , 14 ]. Cancer stem cells (CSCs) are a crucial subpopulation within tumors, known for their ability to self-renew, differentiate, and initiate tumor growth and metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…One mechanism contributing to treatment survival and disease relapse is the presence of cancer stem cells (CSCs) within the tumor tissue. These cells possess pluripotent properties [ 4 ]. CSCs are defined as a subpopulation of tumor cells with the capacity for self-renewal and differentiation to drive the initiation, progression, metastasis, and recurrence of tumors [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

“…CSCs are defined as a subpopulation of tumor cells with the capacity for self-renewal and differentiation to drive the initiation, progression, metastasis, and recurrence of tumors [ 5 ]. There are CSCs that are part of the tissue milieu of the tumor even before the application of therapy, but today, it is well known that even well-differentiated cells are subject to further differentiation in the sense of a shift towards the pluripotent part of the cell spectrum, when CSCs subsequently arise, sometimes paradoxically even in response to the oncological treatment applied (chemo or radiotherapy) [ 4 ]. Today, markers have even been discovered on the cell surface that can identify CSCs, which can be an important therapeutic target, such as CD44 (CD44high) combined with the (near-)absence of CD24 (CD24low) [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Modeling 5-FU-Induced Chemotherapy Selection of a Drug-Resistant Cancer Stem Cell Subpopulation

Ramović Hamzagić,

Cvetković,

Gazdić Janković

et al. 2024

Current Oncology

View full text Add to dashboard Cite

(1) Background: Cancer stem cells (CSCs) are a subpopulation of cells in a tumor that can self-regenerate and produce different types of cells with the ability to initiate tumor growth and dissemination. Chemotherapy resistance, caused by numerous mechanisms by which tumor tissue manages to overcome the effects of drugs, remains the main problem in cancer treatment. The identification of markers on the cell surface specific to CSCs is important for understanding this phenomenon. (2) Methods: The expression of markers CD24, CD44, ALDH1, and ABCG2 was analyzed on the surface of CSCs in two cancer cell lines, MDA-MB-231 and HCT-116, after treatment with 5-fluorouracil (5-FU) using flow cytometry analysis. A machine learning model (ML)–genetic algorithm (GA) was used for the in silico simulation of drug resistance. (3) Results: As evaluated through the use of flow cytometry, the percentage of CD24-CD44+ MDA-MB-231 and CD44, ALDH1 and ABCG2 HCT-116 in a group treated with 5-FU was significantly increased compared to untreated cells. The CSC population was enriched after treatment with chemotherapy, suggesting that these cells have enhanced drug resistance mechanisms. (4) Conclusions: Each individual GA prediction model achieved high accuracy in estimating the expression rate of CSC markers on cancer cells treated with 5-FU. Artificial intelligence can be used as a powerful tool for predicting drug resistance.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Modeling 5-FU-Induced Chemotherapy Selection of a Drug-Resistant Cancer Stem Cell Subpopulation

Ramović Hamzagić,

Cvetković,

Gazdić Janković

et al. 2024

Current Oncology

View full text Add to dashboard Cite

show abstract

“…Based on the obtained results, it is reasonable to conclude that carboplatin did not operate properly in the first 24 h of the cell viability test; the explanation for this may be found in the mechanism of carboplatin action. Because in the mentioned test, a fixed number of cells are seeded, which by inhibiting their proliferation in the first 24 h after sticking (something equivalent to half the rate of duplication of MDA-MB-231 cells in ~ 42 h) 53 cannot be expected to have a significant effect. However, carboplatin has a greater effect in 48 h, which is nearly similar to the rate of cell duplication (~ 42 h).…”

Section: Discussionmentioning

confidence: 99%

Overcoming the non-kinetic activity of EGFR1 using multi-functionalized mesoporous silica nanocarrier for in vitro delivery of siRNA

Parnian

Ma’mani

Bakhtiari

et al. 2022

Sci Rep

View full text Add to dashboard Cite

Triple-negative breast cancer (TNBC) does not respond to HER2-targeted and hormone-based medicines. Epidermal growth factor receptor 1 (EGFR1) is commonly overexpressed in up to 70% of TNBC cases, so targeting cancer cells via this receptor could emerge as a favored modality for TNBC therapy due to its target specificity. The development of mesoporous silica nanoparticles (MSNs) as carriers for siRNAs remains a rapidly growing area of research. For this purpose, a multi-functionalized KIT-6 containing the guanidinium ionic liquid (GuIL), PEI and PEGylated folic acid (FA-PEG) was designed. Accordingly, KIT-6 was fabricated and modified with FA-PEG and PEI polymers attached on the surface and the GuIL placed in the mesopores. Subsequent to confirming the structure of this multi-functionalized KIT-6- based nanocarrier using TEM, SEM, AFM, BET, BJH, DLS and Zeta Potential, it was investigated for uploading and transferring the anti-EGFR1 siRNAs to the MD-MBA-231 cell line. The rate of cellular uptake, cellular localization and endolysosomal escape was evaluated based on the fluorescent intensity of FAM-labelled siRNA using flowcytometry analysis and confocal laser scanning microscopy (CLSM). The 64% cellular uptake after 4 h incubation, clearly suggested the successful delivery of siRNA into the cells and, CLSM demonstrated that siRNA@[FA-PEGylated/PEI@GuIL@KIT-6] may escape endosomal entrapment after 6 h incubation. Using qPCR, quantitative evaluation of EGFR1 gene expression, a knockdown of 82% was found, which resulted in a functional change in the expression of EGFR1 targets. Co-treatment of chemotherapy drug “carboplatin” in combination with siRNA@[FA-PEGylated/PEI@GuIL@KIT-6] exhibited a remarkable cytotoxic effect in comparison to carboplatin alone.

show abstract

“…PCSCs are distinguished from PCa cells by their ability to differentiate uncontrollably, self-renewability, stemness, and quiescence. On the other hand, cancer stem cells (CSCs) divide symmetrically to produce a clone of two CSCs or asymmetrically to produce one CSC and another differentiated form that becomes part of the tumor. , Although evidence suggests the origin of CSCs, its ability to initiate tumors, or the degree to which CSCs can influence tumorigenesis is uncertain, and studies have shown that CSCs are involved in tumor relapse, migration, and resistance toward therapy. − In fact, the plasticity of PCSCs essentially plays a bigger part in bone metastases of PCa. , …”

Section: Introductionmentioning

confidence: 99%

Signaling Pathways and Targeted Therapies for Stem Cells in Prostate Cancer

Giridharan

Rupani

Banerjee

2022

ACS Pharmacol. Transl. Sci.

View full text Add to dashboard Cite

Prostate cancer (PCa) is one of the most frequently occurring cancers among men, and the current statistics show that it is the second leading cause of cancer-related deaths among men. Over the years, research in PCa treatment and therapies has made many advances. Despite these efforts, the standardized therapies such as radiation, chemotherapy, hormonal therapy and surgery are not considered completely effective in treating advanced and metastatic PCa. In most situations, fast-dividing tumor cells are targeted, leaving behind relatively slowly dividing, chemoresistant cells known as cancer stem cells. Therefore, following the seemingly successful treatments, the lingering quiescent cancer stem cells are able to renew themselves, undergo differentiation into mature tumor cells, and sufficiently reinitiate the disease, leading to cancer relapse. Thus, prostate cancer stem cells (PCSCs) have been reported to play a vital role in controlling the dynamics of tumorigenesis, progression, and resistance to therapies in PCa. However, the complete knowledge on the mechanisms regulating the stemness of PCSCs is still unclear. Thus, studying the stemness of PCSCs will allow for the development of more effective cancer therapies due to the durable response, resulting in a reduction in recurrences of cancer. In this Review, we will specifically describe the molecular mechanisms responsible for regulating the stemness of PCSCs. Furthermore, current developments in stem cell-specific therapeutic approaches along with future prospects will also be discussed.

show abstract

Biological characteristics of a sub-population of cancer stem cells from two triple-negative breast tumour cell lines

Abstract: Biological characteristics of a subpopulation of cancer stem cells from two triple-negative breast tumour cell lines, HELIYON,

Cited by 14 publications

References 33 publications

Modeling 5-FU-Induced Chemotherapy Selection of a Drug-Resistant Cancer Stem Cell Subpopulation

Modeling 5-FU-Induced Chemotherapy Selection of a Drug-Resistant Cancer Stem Cell Subpopulation

Overcoming the non-kinetic activity of EGFR1 using multi-functionalized mesoporous silica nanocarrier for in vitro delivery of siRNA

Signaling Pathways and Targeted Therapies for Stem Cells in Prostate Cancer

Contact Info

Product

Resources

About