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DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

ABSTRACT: DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

PROVIDER: PRJNA707567 | ENA |

REPOSITORIES: ENA

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DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

Project description:Growing evidence suggests that cisplatin and other chemotherapeutic agents promote tumor me-tastasis while inhibiting tumor growth, which is a critical issue in clinical practices. However, the role of chemotherapeutics in promoting tumor metastasis and the molecular mechanism involved are unclear. Here, we investigated the roles of cisplatin in promoting tumor metastasis in lung adenocarcinoma (LUAD). We demonstrated that cisplatin promoted epithelial-mesenchymal transition (EMT), cell motility, and metastasis in vitro and in vivo. The bioinformatic analysis and molecular biology approaches also indicated that DCBLD2 is a key gene that mediates cispla-tin-induced metastasis. DCBLD2 stabilizes β-catenin by phosphorylating GSK3β and transporting accumulated β-catenin to the nucleus to promote the expression of EMT-related transcriptional factors (TFs), ultimately resulting in tumor metastasis. We also identified that cisplatin aggravated DCBLD2 expression by phosphorylating ERK and hence the AP-1-driven transcription of DCBLD2. Furthermore, DCBLD2-specific siRNAs encapsulated by nanocarriers prominently in-hibits cisplatin-induced metastasis in vivo. Therefore, DCBLD2 plays a key role in cispla-tin-induced metastasis in LUAD and is a potential target for preventing chemotherapy-induced metastasis in vivo.

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Project description: Not available

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KIAA1522 mediates resistance to cisplatin in lung adenocarcinoma cells

Project description:KIAA1522 is aberrantly over-expressed and predicts the outcome of platinum-base chemotherapy. Down-regulation of KIAA1522 sensitizes lung adenocarcinoma cells to cisplatin. To evaluate the molecular mechanisms underlying KIAA1522-induced cisplatin resistance. The RNA sequencing assays were performed in KIAA1522-depleted 889 cells.

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STAT3 contributes to cisplatin resistance, modulating EMT markers and the mTOR signaling in lung adenocarcinoma cells .

Project description:Lung cancer is the second leading cause of cancer death worldwide and is strongly associated with cisplatin resistance. The transcription factor STAT3 is constitutively activated in cancer cells and coordinates critical cellular processes as survival, self-renewal, and inflammation. In several types of cancer, STAT3 controls the development, immunogenicity, and malignant behavior of tumor cells while dictates the responsiveness to radio- and chemotherapy. It is known that STAT3 phosphorylation on Ser727 by mTOR is necessary for its maximal activation, but the crosstalk between STAT3 and mTOR signaling in cisplatin resistance remains elusive. In this study, using a proteomic label-based approach, we reveal important targets and signaling pathways increased and decreased in cisplatin-resistant A549 lung adenocarcinoma cells.

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ZSWIM1 promotes the proliferation and metastasis of lung adenocarcinoma cells through the STK38/MEKK2/ERK1/2 axis

Project description:Investigating the functions of the proteins with no or less functional annotations is an important goal of C-HPP (Chromosome-centric Human Proteome Project). In this study, we investigated the function of such a protein, ZSWIM1 (C20orf162). Its expression is upregulated in lung adenocarcinoma compared with the adjacent normal tissues and negatively correlated with the overall survival (OS). Overexpressing ZSWIM1 markedly promotes the proliferation, migration, invasion as well as epithelial-mesenchymal transition (EMT) in lung adenocarcinoma cells, while knocking down ZSWIM1 functions oppositely. Immunoprecipitation-mass spectrometry (IP-MS) identified the interactome of ZSWIM1 and we verified the interaction of it with the top partner, STK38. ZSWIM1 antagonized the function of STK38. Mechanically, ZSWIM1 promoted the activation of MEKK2/ERK1/2 pathway through interacting with STK38, leading to the release of MEKK2. Taken together, ZSWIM1 can be annotated as an oncogene in lung adenocarcinoma, and the STK38/MEKK2/ERK1/2 axis mediates its promoting role on lung adenocarcinoma.

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