Proteomic Profiling of Cisplatin-Resistant and Sensitive MDA-MB-231 Triple-Negative Breast Cancer Cell Lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens (human)
SUBMITTER: Prof. Sanjeeva Srivastava
PROVIDER: PXD062652 | JPOST Repository | Tue Apr 07 00:00:00 BST 2026
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SP_CisR1.raw | Raw | |||
| SP_CisR2.raw | Raw | |||
| SP_CisR3.raw | Raw | |||
| SP_CisS1.raw | Raw | |||
| SP_CisS2.raw | Raw |
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Project description:This dataset presents data-independent acquisition (DIA)-based proteomic profiles generated using a timsTOF Pro mass spectrometer for cisplatin-resistant (cisR) and cisplatin-sensitive (cisS) MDA-MB-231 triple-negative breast cancer (TNBC) cell lines. The objective was to decipher proteomic alterations associated with cisplatin resistance. The analysis uncovered significant upregulation of extracellular matrix (ECM) remodeling proteins (e.g., COL6A1, COL6A2, COL6A3), and invasion-related membrane proteins (e.g., TIMP1, MMP-14, APP) in cisR cells. The dataset offers high-resolution, reproducible proteomic insights into the mechanisms of cisplatin resistance, emphasizing the role of EMT, metabolic reprogramming, and membrane remodeling in TNBC.
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Project description:Triple negative breast cancer (TNBC) is an aggressive breast cancer subtype that promotes higher risk of metastasis and cancer reoccurrence, subsequently reduces survival rate of cancer patients. Cisplatin is one of the potential anticancer drugs for treating TNBC. However, occurrence of cisplatin resistance still remains as one of the challenges to fully eradicate TNBC. Since presence of cancer stem cells (CSCs) often known as one of the contributors of drug resistance, investigation has been conducted, suggesting sorted CSC-like subpopulation to be more resistant to cisplatin as compared to parental cells, alongside with higher self-renewability. On the other hand, plethora evidences showed the transmission of exosomal-miRNAs are capable of promoting drug resistance in breast cancers. In this study, we aim to elucidate the differential expression of exosomal-microRNAs profile and reveal the potential target genes in correlation to cisplatin resistance associated with CSC-like subpopulation by using TNBC cell line (MDA-MB-231). Utilizing next generation sequencing and Nanostring techniques, cisplatin-induced dysregulation of exosomal-miRNAs were evaluated in maximal for CSC-like subpopulation as compared to parental cells. Intriguingly, cisplatin induced a relatively oncogenic exosomal-miRNAs profile derived from treated CSC-like subpopulation as compared to treated parental cells, which may correlate to enhancement of drug resistance and maintenance of CSCs. Among the detected exosomal-miRNA profile in treated CSC-like subpopulation, unique clusters of miRNAs namely miR-221-3p, miR-196a-5p, miR-17-5p and miR-126-3p were predicted to target on six genes (ATXN1, LATS1, GSK3β, ITGA6, JAG1 and MYC), aligned with previous finding which demonstrated dysregulation of these genes in treated CSC-like subpopulation. Our results highlight the potential correlation of exosomal-miRNAs and their target genes as well as novel perspectives of the corresponding pathways that may be essential to contribute to the attenuated cytotoxicity of cisplatin in CSC-like subpopulation.
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Project description:BackgroundBreast cancer remains a leading cause of death in women worldwide. Although breast cancer therapies have greatly advanced in recent years, many patients still develop tumour recurrence and metastasis, and eventually succumb to the disease due to chemoresistance. Citral has been reported to show cytotoxic effect on various cancer cell lines. However, the potential of citral to specifically target the drug resistant breast cancer cells has not yet been tested, which was the focus of our current study.MethodsThe cytotoxic activity of citral was first tested on MDA-MB-231 cells in vitro by MTT assay. Subsequently, spheroids of MDA-MB-231 breast cancer cells were developed and treated with citral at different concentrations. Doxorubicin, cisplatin and tamoxifen were used as positive controls to evaluate the drug resistance phenotype of MDA-MB-231 spheroids. In addition, apoptosis study was performed using AnnexinV/7AAD flowcytometry. Aldefluor assay was also carried out to examine whether citral could inhibit the ALDH-positive population, while the potential mechanism of the effect of citral was carried out by using quantitative real time- PCR followed by western blotting analysis.ResultsCitral was able to inhibit the growth of the MDA-MB-231 spheroids when compared to a monolayer culture of MDA-MB-231 cells at a lower IC50 value. To confirm the inhibition of spheroid self-renewal capacity, the primary spheroids were then cultured to additional passages in the absence of citral. A significant reduction in the number of secondary spheroids were formed, suggesting the reduction of self-renewal capacity of these aldehyde dehydrogenase positive (ALDH+) drug resistant spheroids. Moreover, the AnnexinV/7AAD results demonstrated that citral induced both early and late apoptotic changes in a dose-dependent manner compared to the vehicle control. Furthermore, citral treated spheroids showed lower cell renewal capacity compared to the vehicle control spheroids in the mammosphere formation assay. Gene expression studies using quantitative real time PCR and Western blotting assays showed that citral was able to suppress the self-renewal capacity of spheroids and downregulate the Wnt/β-catenin pathway.ConclusionThe results suggest that citral could be a potential new agent which can eliminate drug-resistant breast cancer cells in a spheroid model via inducing apoptosis.
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