Tumour Stem Cells in Breast Cancer

Ибрагимова, М. К.; Цыганов, М. М.; Litviakov, N. V.

doi:10.3390/ijms23095058

Cited by 17 publications

(12 citation statements)

References 181 publications

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“…CSCs are the initiating Cells of tumor formation. It is also called "tumor initiating cells" (TICs) 10 .…”

Section: Discussionmentioning

confidence: 99%

Carboxypeptidase A4 regulates stemness and epithelial-mesenchymal transition in triple-negative breast cancer

Li,

Qin,

et al. 2023

Preprint

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To investigate the significance of carboxypeptidase A4 (CPA4) in triple negative breast cancer (TNBC). The expressions of CPA4, stem and epithelial-mesenchymal transition (EMT) related proteins in TNBC were detected by immunohistochemistry. The relationship between CPA4 and clinicopathological parameters in 168 cases of TNBC was analyzed. The effect of si-CPA4 on MDA-MB-231 was observed. The related proteins were detected by Western Blot. The results indicated the CPA4 positive rate in TNBC was 57.14% (96/168), which was significantly higher than that in non-TNBC tissues (37.5%, 15/40) (χ2 = 5.009, P = 0.025). The positive rate of CPA4 in TNBC tissues was significantly higher than that in breast hyperplasia tissues (20%, 4/20) (χ2 = 9.850, P = 0.002). High CPA4 in patients was positively correlated with NANOG (χ2 = 4.205, P = 0.040) and E-cadherin (χ2 = 11.764, P = 0.040). Vimentin (χ2 = 4.797, P = 0.029), EGFR (χ2 = 4.057, P = 0.044). Si-CPA4 inhibited MDA-MB-231 colony formation, sphere forming, migration and invasion, inhibited the expression of ALDH-1, NANOG and Vimentin, but promoted the expression of E-cadherin. We concluded CPA4 might play an important role in TNBC stemness progression and EMT conversion. CPA4 might be an important therapeutic target for TNBC therapy.

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“…CSCs are the initiating Cells of tumor formation. It is also called "tumor initiating cells" (TICs) 10 .…”

Section: Discussionmentioning

confidence: 99%

Carboxypeptidase A4 regulates stemness and epithelial-mesenchymal transition in triple-negative breast cancer

Li,

Qin,

et al. 2023

Preprint

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“…Other than that, dormant stem-cell-like breast cancer cells express autophagy markers, and upon inhibition of autophagy using 3-methyladenine (3-MA), these cells are transformed to active state [ 104 ]. Moreover, doxycycline not only inhibits EMT (epithelial–mesenchymal transition) and stemness markers in breast cancer stem cells but also causes a down-regulation of autophagy activity [ 105 ], suggesting the possibility that autophagy may play a role in stemness [ 106 ].…”

Section: Complex Relationship Between Key Autophagic Proteins and Var...mentioning

confidence: 99%

“…In luminal and HER2-enriched subtypes of breast cancer, similar results are observed, as chemoresistant cells not only have an elevated autophagic activity compared with their drug-sensitive counterparts but inhibition of autophagy also results in the restoration of chemosensitivity [ 107 , 108 , 109 , 110 ]. Further, expression of mesenchymal markers, vimentin, and the stem cell marker CD44 is increased upon autophagic activity in CSCs [ 106 ]. Additionally, self-renewal of a hormone-independent murine breast cancer cell line LM38-LP requires autophagy [ 111 ].…”

Section: Complex Relationship Between Key Autophagic Proteins and Var...mentioning

confidence: 99%

Autophagy and Breast Cancer: Connected in Growth, Progression, and Therapy

Sharma

2023

Cells

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Despite an increase in the incidence of breast cancer worldwide, overall prognosis has been consistently improving owing to the development of multiple targeted therapies and novel combination regimens including endocrine therapies, aromatase inhibitors, Her2-targeted therapies, and cdk4/6 inhibitors. Immunotherapy is also being actively examined for some breast cancer subtypes. This overall positive outlook is marred by the development of resistance or reduced efficacy of the drug combinations, but the underlying mechanisms are somewhat unclear. It is interesting to note that cancer cells quickly adapt and evade most therapies by activating autophagy, a catabolic process designed to recycle damaged cellular components and provide energy. In this review, we discuss the role of autophagy and autophagy-associated proteins in breast cancer growth, drug sensitivity, tumor dormancy, stemness, and recurrence. We further explore how autophagy intersects and reduces the efficacy of endocrine therapies, targeted therapies, radiotherapy, chemotherapies as well as immunotherapy via modulating various intermediate proteins, miRs, and lncRNAs. Lastly, the potential application of autophagy inhibitors and bioactive molecules to improve the anticancer effects of drugs by circumventing the cytoprotective autophagy is discussed.

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“…They highlight non-genetic mechanisms that enable cancer cells to reversibly adapt to their environment, unlike genetic mechanisms that are irreversible, underscoring the dire need to reconcile the two mechanisms. Additionally, plastic phenotypes such as cancer stem cells (CSCs) are also well-recognized entities contributing to drug resistance in many cancers [ 27 , 28 , 29 ]. Therefore, the dynamic heterogeneity and the dynamic transitions between CSCs and non-CSCs and their significance in metastasis and drug resistance warrant a deeper understanding of the underlying mechanisms.…”

Section: Current Treatment Strategies May Be Counterproductivementioning

confidence: 99%

Addressing Drug Resistance in Cancer: A Team Medicine Approach

Kulkarni

Mohanty

Bhattacharya

et al. 2022

JCM

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Drug resistance remains one of the major impediments to treating cancer. Although many patients respond well initially, resistance to therapy typically ensues. Several confounding factors appear to contribute to this challenge. Here, we first discuss some of the challenges associated with drug resistance. We then discuss how a ‘Team Medicine’ approach, involving an interdisciplinary team of basic scientists working together with clinicians, has uncovered new therapeutic strategies. These strategies, referred to as intermittent or ‘adaptive’ therapy, which are based on eco-evolutionary principles, have met with remarkable success in potentially precluding or delaying the emergence of drug resistance in several cancers. Incorporating such treatment strategies into clinical protocols could potentially enhance the precision of delivering personalized medicine to patients. Furthermore, reaching out to patients in the network of hospitals affiliated with leading academic centers could help them benefit from such innovative treatment options. Finally, lowering the dose of the drug and its frequency (because of intermittent rather than continuous therapy) can also have a significant impact on lowering the toxicity and undesirable side effects of the drugs while lowering the financial burden carried by the patient and insurance providers.

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Tumour Stem Cells in Breast Cancer

Cited by 17 publications

References 181 publications

Carboxypeptidase A4 regulates stemness and epithelial-mesenchymal transition in triple-negative breast cancer

Carboxypeptidase A4 regulates stemness and epithelial-mesenchymal transition in triple-negative breast cancer

Autophagy and Breast Cancer: Connected in Growth, Progression, and Therapy

Addressing Drug Resistance in Cancer: A Team Medicine Approach

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