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Examination of microRNA expression in pre- and post-treatment plasma samples of 3 patients

ABSTRACT: Drug resistance often tempers the clinical benefit of chemotherapy in human malignant tumors. The potential chemosensitization of low-dose decitabine has been evident both preclinically and in previous phase I trials. Emerging data showed that miRNAs play an important role as a prognostic factor for cancer survival. Given that the biopsy tumor tissue was often not available, especially for patients with relapsed or refractory cancer, plasma RNA provided a valuable source for biomarker development. In order to establish predictive biomarker signature for the clinical efficacy of the decitabine-primed chemotherapy, we evaluated the expression of plasma miRNAs via high throughput microRNA sequencing. We performed miRNA-seq on a training set of 2 partial response (PR) patients and 1 progressive disease (PD) patients, and revealed preliminary data that plasma miRNA expression signature may serve as putative predictive markers of the low-dose decitabine primed chemotherapy. The clinical responses were assessed in a blinded manner according to the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE91089 | GEO | 2016/12/15

SECONDARY ACCESSION(S): PRJNA356856

REPOSITORIES: GEO

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Project description:A Cytotoxic T lymphocyte-inspired system capable of using ultralow-dose chemical drugs to manipulate cell death is needed to investigate the antitumour immunotherapy. Recent studies revealed pyroptosis, a proinflammatory type of cell death, could promote antitumour immune function. However, high-dose chemotherapy led to cytokine release syndrome by pyroptosis. Therefore, pyroptosis- inducing ultralow-dose chemotherapy was potential in preclinical and clinical research, but its efficacy, safety and the antitumour immune responses were not clear. Here, we established a near-infrared light controllable killing system (BIK system) by which ultralow-dose doxorubicin could be spatiotemporally transported to immunosuppressive tumour cells and mediate efficient pyroptosis. Compared with using DOX directly, the BIK system reduced total drug consumption to less than one- thirtieth the common dose in vitro. MPI imaging and fluorescence imaging showed our BIK system exhibited good tumour targeting and tumour penetration. We applied this system for pyroptosis-induced antitumor therapies, and the results showed that less than 43 µg kg-1 DOX was sufficient for GSDME-positive tumour regression with negligible injuries to major organs. Notably, the gasdermin-deficient 4T1 tumours could be controlled by combining BIK system with decitabine treatment. The antitumour immune function were proven to correlate with the impressive efficacy of pyroptosis-inducing ultralow-dose chemotherapy, and the concomitant immune memory prevented metastasis, but high-dose DOX led to poor T cells infiltration which caused immunosuppression and lung metastasis. Owing to the robust antitumour immune function induced by BIK system, advanced-stage bulky tumours could be controlled or shrunken by synergizing with anti-PD-1 therapy. This study provided new insights into the design of nanoassisted systems for activating the antitumour immune function by microstimulation; our application of the BIK system suggested that ultralow-dose chemotherapy was sufficient for inducing a robust pyroptosis-mediated antitumour immune function

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Examination of microRNA expression in pre- and post-treatment plasma samples of 3 patients

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