Patient-derived primary breast cancer cells and their potential for predicting sensitivity to chemotherapy

Mou, Yajun; Huang, Jianjun; Yang, Wenxiu; Wan, Yu; Pu, Zhenhong; Zhang, Mengjie; Liu, Jinting; Li, Qing; Zhang, Peipei; Tian, Yuan; Yang, Hui; Cui, Yi; Hu, Peng; Dou, Xiaowei

doi:10.3389/fonc.2022.1023391

Cited by 4 publications

(1 citation statement)

References 21 publications

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“…Conversely, although 3D cultures can be initiated with freshly resected and dissociated breast tumors, they are limited in the number of times they can be passaged, and the presence of TIL in these cultures is variable at best 15,18 . Lastly, primary breast cancer cells can be expanded in 2D cultures; however, many of the protocols that are currently available are cumbersome and are focused on generating breast cancer cell cultures only and exclude the autologous CAFs and TILs which are important components of the breast TME [19][20][21] .…”

Section: Introductionmentioning

confidence: 99%

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues

Topolnitska,

Moreno,

Paiva

et al. 2024

Preprint

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Therapy resistance and tumor recurrence are major challenges in the clinical management of breast cancer. Current data indicates that the breast tumor microenvironment (TME) and the tumor immune microenvironment (TIME) are important modulators of breast cancer cell response to chemotherapies and the development of therapy resistance. To this end, the ability to recreate the tumor microenvironment in the laboratory using autologous primary cells that make up the breast TME has become an indispensable tool for cancer researchers as it allows the study of tumor immunobiology in the context of therapy resistance. Moreover, the clinical relevance of data obtained from single cell transcriptomics and proteomics platforms would be greatly improved if primary autologous tumor cells were used. In this article, we report a robust and efficient workflow to obtain autologous cancer cells, cancer-associated fibroblasts, and tumor-infiltrating immune cells from primary human breast cancer tumors obtained from mastectomy procedures. As well, we show that this protocol can be used to obtain normal-like epithelial cells, fibroblasts, and immune cells from the matching tumor-adjacent breast tissue samples. Also, a robust methodology to expand each of these primary cell typesin vitrois presented that allows the maintenance of the primary tumor cell phenotype. The availability of a large number of autologous primary human breast tumor cells and their matching tumor-adjacent tissues will facilitate the study of differential and cancer cell-specific gene expression patterns that will further our understanding of how the TME and TIME influence therapy resistance in the breast tumor context.

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Section: Introductionmentioning

confidence: 99%

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues

Topolnitska,

Moreno,

Paiva

et al. 2024

Preprint

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SNF2L maintains glutathione homeostasis by initiating SLC7A11 transcription through chromatin remodeling

Zhang,

Gao,

Yang

et al. 2024

Cell Death Dis

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SNF2L encodes an ISWI chromatin remodeling factor that promotes gene transcription and is consistently elevated in cancers. Previous studies have shown that inhibiting SNF2L expression in cancer cells leads to significant growth suppression, DNA damage, and cell death. However, the underlying mechanisms remain poorly understood. In this study, we demonstrated that cancer cells lacking SNF2L show significantly decreased glutathione (GSH) levels, leading to elevated reactive oxygen species (ROS) and increased oxidative stress. SNF2L deficiency also heightened the sensitivity of cancer cells to APR-246, a drug that depletes GSH and induces oxidative stress, consequently decreasing cell viability and increasing ROS levels, regardless of p53 status. Mechanistically, we found that NRF2 recruits SNF2L to the SLC7A11 promoter, leading to increased chromatin accessibility and facilitating SLC7A11 transcription. This results in decreased cystine uptake and impaired GSH biosynthesis. These findings suggest that targeting the SNF2L/SLC7A11 axis could enhance the effectiveness of APR-246 by depleting GSH and increasing ROS level in cancer cells, highlighting SNF2L as a promising therapeutic target.

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Tumor-on-chip platforms for breast cancer continuum concept modeling

Neagu,

Whitham,

Bruno

et al. 2024

Front. Bioeng. Biotechnol.

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Our previous article entitled “Proteomics and its applications in breast cancer”, proposed a Breast Cancer Continuum Concept (BCCC), including a Breast Cancer Cell Continuum Concept as well as a Breast Cancer Proteomic Continuum Concept. Breast cancer-on-chip (BCoC), breast cancer liquid biopsy-on-chip (BCLBoC), and breast cancer metastasis-on-chip (BCMoC) models successfully recapitulate and reproduce in vitro the principal mechanisms and events involved in BCCC. Thus, BCoC, BCLBoC, and BCMoC platforms allow for multiple cell lines co-cultivation to reproduce BC hallmark features, recapitulating cell proliferation, cell-to-cell communication, BC cell-stromal crosstalk and stromal activation, effects of local microenvironmental conditions on BC progression, invasion/epithelial-mesenchymal transition (EMT)/migration, intravasation, dissemination through blood and lymphatic circulation, extravasation, distant tissues colonization, and immune escape of cancer cells. Moreover, tumor-on-chip platforms are used for studying the efficacy and toxicity of chemotherapeutic drugs/nano-drugs or nutraceuticals. Therefore, the aim of this review is to summarize and analyse the main bio-medical roles of on-chip platforms that can be used as powerful tools to study the metastatic cascade in BC. As future direction, integration of tumor-on-chip platforms and proteomics-based specific approaches can offer important cues about molecular profile of the metastatic cascade, alowing for novel biomarker discovery. Novel microfluidics-based platforms integrating specific proteomic landscape of human milk, urine, and saliva could be useful for early and non-invasive BC detection. Also, risk-on-chip models may improve BC risk assessment and prevention based on the identification of biomarkers of risk. Moreover, multi-organ-on-chip systems integrating patient-derived BC cells and patient-derived scaffolds have a great potential to study BC at integrative level, due to the systemic nature of BC, for personalized and precision medicine. We also emphasized the strengths and weaknesses of BCoC and BCMoC platforms.

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Patient-derived primary breast cancer cells and their potential for predicting sensitivity to chemotherapy

Cited by 4 publications

References 21 publications

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues

SNF2L maintains glutathione homeostasis by initiating SLC7A11 transcription through chromatin remodeling

Tumor-on-chip platforms for breast cancer continuum concept modeling

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Patient-derived primary breast cancer cells and their potential for predicting sensitivity to chemotherapy

Cited by 4 publications

References 21 publications

A robust protocol for the systematic collection and expansion of cells from ER+breast cancer tumors and their matching tumor-adjacent tissues

A robust protocol for the systematic collection and expansion of cells from ER+breast cancer tumors and their matching tumor-adjacent tissues

SNF2L maintains glutathione homeostasis by initiating SLC7A11 transcription through chromatin remodeling

Tumor-on-chip platforms for breast cancer continuum concept modeling

Contact Info

Product

Resources

About

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues

A robust protocol for the systematic collection and expansion of cells from ER⁺breast cancer tumors and their matching tumor-adjacent tissues