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MUC13-associated molecular interactome in pancreatic cancer

ABSTRACT: MUC13 has emerged as a critical molecular player that is involved in tumorigenesis, cancer progression, metastasis and evade immune surveillance, including in pancreatic cancer. In this report, we have identified MUC13 molecular interactome using an integrated immunoprecipitation and liquid chromatography mass spectrometry (IP-LCMS) technique and systems network biology approach to determine its functional protein-protein interaction network and its associated oncogenic mechanisms. This study reveals total 54 key interactor proteins (CDK1, CTNND1, Caludin-1, ErbB3-binding protein 1, Basic transcription factor 3 and Tight junction protein 1 protein etc) of MUC13. Interestingly majority of the interacting proteins were found to be associated with oncogenic and immune checkpoint pathways. These proteins are involved in the regulation of PD1/PD-L1, T-cell receptor signaling, and post-translational protein processing and modifications in the endoplasmic reticulum. This study also revealed that MUC13 might be involved in other cellular processes such as apoptosis, autophagy, senescence, calcium signaling, microRNA activity, lysosomal function, and diabetic cardiomyopathy. Taken together, this study for the first time elucidated MUC13 associated molecular interactome that might be involved in pancreatic cancer progression and metastasis. This study will help to develop new strategies to intervene pancreatic cancer progression via disrupting MUC13 associated oncogenic molecular network.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Subhash C. Chauhan

PROVIDER: PXD070763 | JPOST Repository | Sat Nov 15 00:00:00 GMT 2025

REPOSITORIES: jPOST

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is a heterogeneous cancer in which differences in survival rates might be related to a variety in gene expression profiles. Although the molecular biology of PDAC begins to be revealed, genes or pathways that specifically drive tumour progression or metastasis are not well understood. Therefore, we performed microarray analyses on whole-tumour samples of 2 human PDAC subpopulations with similar clinicopathological features, but extremely distinct survival rates after potentially curative surgery, i.e., good outcome (OS and DFSM-bM-^@M-^I>M-bM-^@M-^I50M-bM-^@M-^Imonths) versus bad outcome (OSM-bM-^@M-^I<M-bM-^@M-^I19M-bM-^@M-^Imonths and DFSM-bM-^@M-^I<M-bM-^@M-^I7M-bM-^@M-^Imonths). Additionally, liver- and peritoneal metastases were analysed and compared to primary cancer tissue. The integrin and ephrin receptor families were upregulated in all PDAC samples, irrespective of outcome, supporting an important role of the interaction between pancreatic cancer cells and the surrounding desmoplastic reaction in tumorigenesis and cancer progression. Moreover, some components, such as ITGB1 and EPHA2, were upregulated in PDAC samples with a poor outcome, Additionally, overexpression of the non-canonical Wnt/M-NM-2-catenin pathway and EMT genes in PDAC samples with bad versus good outcome suggests their contribution to the invasiveness of pancreatic cancer, with M-NM-2-catenin being also highly upregulated in metastatic tissue. Thus, we conclude that components of the integrin and ephrin pathways and EMT-related genes might serve as molecular markers in pancreatic cancer as their expression seems to be related with prognosis. Microarray analysis was performed on 'Good' and 'Bad' patient samples (samples with similar pathological characteristics were chosen based on the definition of the 2 diverse survival outcome groups and the required RIN values above 7.1), on surrounding non-tumoural pancreatic control samples, liver metastasis (LM) and peritoneal metastasis (PM). Comparisons between good vs. control, bad vs. control, good vs. bad, and primary pancreatic cancer versus metastasis were performed.

			Action	DRS
	Capan2.raw	Raw
	Capan2.xml	Xml
	HIgIP.raw	Raw
	HIgIP.xml	Xml
	HMIP.raw	Raw

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MUC13-associated molecular interactome in pancreatic cancer

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