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TIFA links Aurora A to NF-κB survival pathway to support chemoresistance in acute myeloid leukemia

ABSTRACT: Aberrant secretion of cytokines contributes to pathogenesis of leukemia and is considered a prognostic signature for recurrence of AML. We asked whether molecular targeting of TIFA can perturb NF-κB-dependent secretion of leukemic cytokines and attain better therapeutic efficacy. We performed cytokine antibody array to profile cytokines secreted by U937 cells in response to TIFA dominant-negative fragments and cytarabine treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE87383 | GEO | 2016/11/21

SECONDARY ACCESSION(S): PRJNA344579

REPOSITORIES: GEO

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Paediatric Bone marrow Mesenchymal Stem cells support acute myeloid leukaemia cell survival and enhance chemoresistance via contact-independent mechanism

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B27 modulation of LPS response

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Aurora-A Induces Chemoresistance Through Activation of the AKT/mTOR Pathway in Endometrial Cancer.

Project description:Endometrial cancer (EC) is the most common gynecological tumor all over the world, and advanced/metastatic EC remains a malignancy with poor survival outcome due to highly resistant to conventional chemotherapeutic treatment. Here, we report that Aurora-A, a serine-threonine kinase, plays a vital role in chemoresistance of EC. Aurora-A is overexpressed in EC tissues, compared with normal endometrium and Aurora-A expression is associated with decreased overall survival. Overexpression of Aurora-A in EC cell lines (Ishikawa and HEC-1B cells) promotes cell proliferation and induced paclitaxel- and cisplatin-resistance. Furthermore, Aurora-A activating AKT-mTOR pathway further induces chemoresistance in vitro, consistent with a positive correlation between Aurora-A and phosphorylated AKT/4E-BP1 expression in EC tissues. In summary, our study provides the strong evidence that Aurora-A controls the sensitivity of EC cell lines to chemotherapy via AKT/mTOR pathway, indicating that pharmacologic intervention of Aurora-A and AKT/mTOR in combination with chemotherapy may be considered for the targeted therapy against EC with overexpression of Aurora-A.

| S-EPMC6540875 | biostudies-literature

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