Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative Mass Spectrometry-Based Profiling of Cell Surface and Crude Membrane Proteins in Cisplatin-Resistant Triple-Negative Breast Cancer Cells

ABSTRACT: This dataset includes cell surface (CSP) and crude membrane (CM) proteomic profiles of cisplatin-resistant and sensitive triple-negative breast cancer (TNBC) cell lines generated using data-independent acquisition (DIA) mass spectrometry workflows. Surface proteins were selectively enriched using membrane-impermeable biotinylation and affinity purification, while crude membrane proteins were isolated through differential ultracentrifugation. LC-MS/MS analysis was performed to identify and quantify differentially expressed proteins associated with cisplatin resistance. The dataset provides valuable insights into altered surfaceome and membrane proteome dynamics that underlie drug resistance mechanisms in TNBC, and highlights potential biomarkers and therapeutic targets for overcoming chemoresistance.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Prof. Sanjeeva Srivastava

PROVIDER: PXD064232 | JPOST Repository | Sat May 23 00:00:00 BST 2026

REPOSITORIES: jPOST

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	CM_R1.d.rar	Other
	CM_R2.d.rar	Other
	CM_R3.d.rar	Other
	CM_S1.d.rar	Other
	CM_S2.d.rar	Other

Items per page:

1 - 5 of 17

Similar Datasets

TimsTOF-Based DIA Proteomic Profiling of Cisplatin-Resistant and Sensitive MDA-MB-231 Triple-Negative Breast Cancer Cell Lines

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.

2026-04-22 | PXD063175 | JPOST Repository

Proteomic Profiling of Cisplatin-Resistant and Sensitive MDA-MB-231 Triple-Negative Breast Cancer Cell Lines

Project description:This dataset includes mass spectrometry-based proteomic profiles of cisplatin-resistant (cisR) and cisplatin-sensitive (cisS) MDA-MB-231 triple-negative breast cancer (TNBC) cell lines. The study aimed to investigate the molecular alterations contributing to cisplatin resistance using data-independent acquisition (DIA) proteomics. Key findings revealed upregulation of extracellular matrix (ECM) remodeling proteins (e.g., COL6A1, COL6A3), drug efflux transporters (e.g., ABCC4), and membrane-associated resistance proteins (e.g., TIMP1, MMP-14, APP), highlighting their potential roles in chemoresistance. The data provide insights into resistance-associated signaling, metabolic pathways, and potential therapeutic targets in TNBC.

2026-04-07 | PXD062652 | JPOST Repository

Cisplatin-induced gene expression changes in triple-negative breast cancer (TNBC) cells

Project description:Breast cancers lacking receptors for estrogen, progesterone or HER2 on their cell surface are called triple-negative breast cancers (TNBCs). TNBCs account for ~15-20% of all invasive breast cancers and do not benefit from anti-hormonal or anti-HER2 treatments. Although patients with TNBC can initially respond to chemotherapy, they do have worse overall prognosis compared to other breast cancer subtypes. Unfortunately, TNBCs lack clear targetable ‘driver’ oncogenes. Thus, there is an unmet need for strategies to improve the therapeutic options for these patients. We used microarrays to assess differences in gene expression in triple-negative breast cancer cells in response to the platinum-based chemotherapeutic agent cisplatin. The purpose was to find drug induced changes in gene expression level that could differentiate cisplatin sensitive from cisplatin resistant TNBC cell lines.

2017-08-26 | GSE103115 | GEO

ATP6V0D2 drives triple-negative breast cancer progression and inhibits cisplatin sensitivity by promoting PHLPP2 lysosomal degradation

Project description:Triple-negative breast cancer (TNBC) faces therapeutic challenges due to limited treatment options and frequent chemoresistance. In this study, we identify ATP6V0D2 as a key factor upregulated in TNBC, where its expression correlates with poor prognosis. Transcriptomic and functional analyses linked ATP6V0D2 to PI3K/AKT signaling and platinum drug resistance. Mechanistically, ATP6V0D2 enhanced lysosomal function to promote degradation of the tumor suppressor PHLPP2, thereby sustaining AKT phosphorylation. Functional assays showed that ATP6V0D2 knockdown increased cisplatin sensitivity both in vitro and in vivo. Furthermore, pharmacological inhibition of V-ATPase with bafilomycinA1 sensitized TNBC patient-derived organoids to cisplatin. Clinically, our analysis of 91 TNBC patients who received cisplatin-based neoadjuvant chemotherapy found that high ATP6V0D2 expression was inversely correlated with pathological complete response (pCR), whereas PHLPP2 levels showed positive association, supporting the proposed mechanistic link. Together, these findings highlight the impact of ATP6V0D2 on TNBC progression and cisplatin sensitivity, nominating ATP6V0D2 as a promising therapeutic target.

2025-12-09 | GSE309752 | GEO

Tumor expression data from neoadjuvant trial of cisplatin monotherapy in triple negative breast cancer patients

Project description:Evidence suggests that BRCA1 mutation associated tumors have increased sensitivity to DNA damaging agents like cisplatin. Sporadic triple negative breast cancers (TNBC) have many phenotypic similarities to BRCA1 tumors and may have a similar sensitivity to cisplatin. We tested the efficacy of cisplatin monotherapy in 28 TNBC patients in a single arm neoadjuvant trial with outcome measured by pathologic treatment response quantified using the Miller-Payne scale. We used microarrays gene expression profiles to determine tumor subtype of each trial tumor sample and to test various expression signatures for association with pathologic response to cisplatin. Pretreatment tumor samples from the clinical trial (N=24 with adequate tissue) were used for RNA extraction, linear amplification, biotin labeling and hybridization to Affymetrix U133 plus 2.0 arrays. A reference set of 51 primary breast tumors representing all subtypes of breast cancer were processed in a similar manner to include linear amplification, and hybridized to Affymetrix arrays.

2009-11-04 | E-GEOD-18864 | biostudies-arrayexpress

Tumor expression data from neoadjuvant trial of cisplatin monotherapy in triple negative breast cancer patients

2009-11-04 | GSE18864 | GEO

MiR-302b as a Combinatorial Therapeutic Approach to Improve Cisplatin Chemotherapy Efficacy in Human Triple Negative Breast Cancer

Project description:Chemotherapy is still the standard–of-care for triple-negative breast cancers (TNBCs). Here, we investigated miR-302b as therapeutic tool to enhance cisplatin sensitivity in vivo and unraveled the molecular mechanism. Material and method: TNBC xenografted mice were treated with miR-302b or control, alone or with cisplatin. Genome-wide transcriptome analysis and independent-validation of ITGA6 expression was assessed on mice tumor samples. SiRNA-knockdown of ITGA6 was performed to evaluate cisplatin response in vitro. Further, potential transcription factors of ITGA6 (E2F1, E2F2 and YY1) were explored to define the miRNA molecular mechanism. MiR-302b expression was also assessed in TNBC patients treated with chemotherapy. Results: MiR-302b-cisplatin combination significantly impaired tumor growth versus control, through indirect ITGA6 downregulation. Indeed, ITGA6 was downmodulated in mice treated with miR-302b-cisplatin and ITGA6 silencing increased drug sensitivity in TNBC cells. In silico analyses and preclinical assays pointed out the regulatory role of E2F family and YY1 on ITGA6 expression under miR-302b-cisplatin treatment. Finally, miR-302b enrichment correlates with better overall survival in 118 TNBC patients. Conclusion: MiR-302b can be exploited as a new therapeutic tool to improve the response to chemotherapy, modulating E2F family, YY1 and ITGA6 expression. Moreover, miR-302b could be defined as new prognostic factor in TNBC patients.

2020-08-21 | GSE152322 | GEO

PProteomic analysis of enhanced cellular effects of electroporation and cisplatin in triple-negative breast cancer cells

Project description:We performed a comprehensive and label-free quantitative proteomic analysis of the human adenocarcinoma epithelial TNBC cells (MDA-MB-231) treated with Cisplatin (CsP) and Cisplatin with EP (EP+CsP). We identified hundreds of differentially expressed proteins that defines molecular mechanisms involved in cellular responses of MDA-MB-231 cells to ECT. The underlying dataset represents a valuable resource for mechanistic studies and for the validation of knowledge gained from this study in the future using animal models. The systemic data should build a foundation for a better understanding of the mechanisms of the cytotoxicity of the Cisplatin as a potent anticancer drug.

2019-01-24 | MSV000083360 | MassIVE

Olaparib resistance and cisplatin responses in triple negative breast cancer

Project description:PARP inhibitor and platinum based drugs such as cisplatin are promising therapies for triple negative breast cancer and exploit the deficiencies in BRCA1 or BRCA2, or homologous recombination repair defects. However, PARP inhibitor resistance is proven to be a major clinical problem. Acquired PARP inhibitor resistance has been linked with co-resistance to platinum-based drugs. To determine how acquired olaparib resistance affects cisplatin response and whether this is influenced by their BRCA1 status, we performed RNAseq transcriptome analysis of isogenic triple negative breast cancer models of olaparib resistance with normal and mutant BRCA1.

2021-07-22 | GSE165914 | GEO

Transcriptional profiling of ovarian cancer spheroids reveals genes and related biological pathways associated with cisplatin resistance

Project description:Characterization of differential gene expression due to cisplatin resistance in human ovarian cancer spheroids by microarray analysis. In this dataset, we include the expression data obtained from cisplatin-sensitive and cisplatin-resistant human ovarian cancer spheroids. These data are used to obtain 1316 genes that are differentially expressed in response to cisplatin resistance.

2015-12-01 | GSE45553 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data