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

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

PROVIDER: PRJNA638955 | ENA |

REPOSITORIES: ENA

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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

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

Project description:Introduction: Chemotherapy is still the standard of care for triple-negative breast cancers (TNBCs). Here, we investigated miR-302b as a therapeutic tool to enhance cisplatin sensitivity in vivo and unraveled the molecular mechanism. Materials and Methods: TNBC-xenografted mice were treated with miR-302b or control, alone or with cisplatin. Genome-wide transcriptome analysis and independent-validation of Integrin Subunit Alpha 6 (ITGA6) expression was assessed on mice tumor samples. Silencing of ITGA6 was performed to evaluate cisplatin response in vitro. Further, potential transcription factors of ITGA6 (E2F transcription facor 1 (E2F1), E2F transcription factor 2 (E2F2), and Yin Yang 1 (YY1)) were explored to define the miRNA molecular mechanism. The miR-302b expression was also assessed in TNBC patients treated with chemotherapy. Results: The miR-302b-cisplatin combination significantly impaired tumor growth versus the 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 the E2F family and YY1 on ITGA6 expression under miR-302b-cisplatin treatment. Finally, miR-302b enrichment correlated 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 the E2F family, YY1, and ITGA6 expression. Moreover, miR-302b could be defined as a new prognostic factor in TNBC patients.

| S-EPMC7464985 | biostudies-literature

Therapeutic potential for reversing miR-634-mediated cytoprotective processes to improve the efficacy of chemotherapy against oral squamous cell carcinoma

Project description:For advanced oral squamous cell carcinoma (OSCC), increasing sensitivity to chemotherapy is a major challenge in improving treatment outcomes, and targeting cytoprotective processes that lead to the chemotherapy resistance of cancer cells may be therapeutically promising. Tumor-suppressive microRNAs (miRs) can target multiple cancer-promoting genes concurrently, and are thus expected to be useful seeds for cancer therapeutics. We revealed that miR-634-meditated targeting of multiple cytoprotective process-related genes, including cellular inhibitor of apoptosis proteins 1 (cIAP1), can effectively increase cisplatin (CDDP)-induced cytotoxicity and overcome CDDP resistance in OSCC cells. The combination of topical treatment with miR-634 ointment and administration of CDDP was synergistically effective against OSCC-tumor growth in a xenograft mouse model. Furthermore, the expression of miR-634 target genes is frequently upregulated in primary OSCC tumors. Our study suggests that reversing miR-634-mediated cytoprotective processes activated in cancer cells is a potentially useful strategy to improve CDDP efficacy against advanced OSCC.

2022-05-25 | GSE194269 | GEO

Identification of a biomarker to predict doxorubicin/cisplatin chemotherapy efficacy for osteosarcoma patients by 4D data-independent acquisition (DIA) mass spectrometry with parallel reaction monitoring (PRM) verification

Project description:We analyzed the differentially expressed proteins in 37 resected tissue samples from osteosarcoma patients using paraffin- embedded specimens and 4D data-independent acquisition (DIA) quantitative mass spectrometry to investigate biomarkers for predicting the efficacy of doxorubicin/cisplatin chemotherapy

2024-10-17 | PXD051097 | Pride

Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients

Project description:There is large variability among lung squamous cell carcinoma (SCC) patients in response to treatment with cisplatin based chemotherapy. LncRNAs is potentional a new type of predictive marker that can identify subgroups of patients who benefit from chemotherapy and it will have great value for treatment guidance. Differentially expressed LncRNAs were identified using microarray profiling of tumors with partial response (PR) vs. with progressive disease (PD) from advanced lung SCC patients treated with cisplatin based chemotherapy and validated by quantitative real-time PCR (qPCR). Results: Compared with the PD samples, 953 lncRNAs were consistently overregulated and 749 lncRNAs

2015-05-18 | E-GEOD-59245 | biostudies-arrayexpress

Combinatorial Treatment of Poly (ADP-ribose) Polymerase-1 Inhibitors and Cisplatin Attenuates Cervical Cancer Growth Through FOS-Driven Changes in Gene Expression

Project description:Cervical cancer is the one of the most prevalent types of cancers in women and is the second highest cause of death in women aged 20-39. The most common chemotherapy for cervical cancer involves the use of the drug cisplatin in conjunction with other therapeutics. However, the development of cisplatin resistance in patients can hinder the efficacy of these treatments. This highlights the need to explore different therapeutic approaches for cervical cancer treatment. We found that inhibitors targeting the enzyme Poly (ADP-ribose) Polymearse (PARP)-1 can attenuate cell growth of cervical adenocarcinoma and squamous cell carcinoma. Furthermore, combinatorial therapy of PARP inhibitors (PARPi) with cisplatin increases the cisplatin-mediated cell toxicity in cervical cancer cells. This is accompanied by a rewiring of the transcriptome in response to the cisplatin and PARPi together. Surprisingly, we observed that the Fos gene is upregulated in the dual treatment condition leading to the subsequent induction of its target genes. Importantly, increased the expression of Fos is sufficient to hinder cervical cancer growth. We conclude that by inducing Fos expression, PARPi treatment with cisplatin leads to inhibition of cervical cancer.

2022-08-02 | GSE176326 | GEO

Clinical response of metastatic gastric cancer patients to cisplatin and fluorouracil (CF) combination chemotherapy

2011-06-01 | GSE14208 | GEO

Clinical response of metastatic gastric cancer patients to cisplatin and fluorouracil (CF) combination chemotherapy

Project description:This study was conducted to identify transcriptional profiles predictive of a clinical response of metastatic gastric cancer patients to cisplatin and fluorouracil (CF) combination chemotherapy. Endoscopic biopsy samples were collected from CF-treated metastatic gastric cancer patients prior to therapy and following the development of resistance to therapy.

2011-06-01 | E-GEOD-14208 | biostudies-arrayexpress

MEK Inhibition Overcomes Cisplatin Resistance Conferred by SOS/MAPK Pathway Activation in Squamous Cell Carcinoma (SCC)

Project description:Genomic analyses of SCC have yet to yield significant strategies against pathway activation to improve treatment. Platinum-based chemotherapy remains the mainstay of treatment for SCC of different histotypes either as a single agent or alongside other chemotherapeutic drugs or radiotherapy; however, resistance inevitably emerges, which limits the duration of treatment response. To elucidate mechanisms that mediate resistance to cisplatin, we compared drug-induced perturbations to gene expression between cisplatin-sensitive and -resistant SCC cells. Cisplatin-sensitive and -resistant SCC cells were identified through MTS assay. Gene expression profiling (Affymetrix GeneChip 1.0ST) was performed to identify putative genes and cellular pathways that may be associated with cellular response to cisplatin.

2015-08-05 | E-GEOD-66549 | biostudies-arrayexpress

RT-PCR profiling analysis of microRNA expression in cisplatin-resistant cancer

Project description:Chemotherapy remains the primary treatment of advanced solid cancer, including lung cancer. As first line treatment, cisplatin-based therapy is restricted by frequent development of drug resistance. Increasing data showed that programmed cell death protein ligand 1 (PD-L1) plays a vital role in regulating cisplatin resistance. However, the mechanisms underlying are not fully understood. We found miR-526b-3p expression declined while PD-L1 elevated in cisplatin-resistant lung cancer compared to that in cisplatin-sensitive lung cancer by analyzing clinical samples. Importantly, miR-526b-3p was associated with response to cisplatin negatively. We further demonstrated that miR-526b-3p reversed cisplatin resistance, suppressed metastasis, and activated CD8+ T cells in a STAT3/PD-L1-dependent manner. Our findings extended the knowledge of PD-L1-mediated cisplatin resistance of lung cancer. In addition, the introduction of miR-526b-3p provided a new clue to improve the anti-tumor effects of the combination of immunotherapy and chemotherapy. miProfileTM Cancer miRNA qPCR Array

2021-03-12 | GSE168707 | GEO

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