Proteomics

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Neurochondrin Drives Colorectal Cancer Progression by Modulating the PODXL–Ezrin Axis and Mitochondrial Function


ABSTRACT: Neurochondrin (NCDN) has been recently identified as upregulated in metastatic to liver KM12SM colorectal cancer (CRC) cells in comparison to the poorly metastatic KM12C CRC cells. Furthermore, high levels of NCDN in patients correlate to a worse survival. In this work, using an independent patient cohort, we validated the worsened prognosis associated to NCDN’s elevated levels. Then, we sought to investigate the role of NCDN in CRC progression using the isogenic KM12 CRC cell model comprised of the aforementioned KM12C and KM12SM cells. Stable silencing of NCDN in both cell lines produced a reduction on the tumorigenic capacities of the cells in vitro as seen through different assays (proliferation, adhesion, colony formation…). In vivo, mice injected with the silenced cells had impaired tumor growth and metastasis compared to mice injected with the control cells. Proteomic profiling of NCDN-silenced cells uncovered a set of dysregulated proteins associated with NCDN such as PODXL, indicating that the NCDN-PODXL axis constitutes a critical mediator of CRC liver metastasis. Our findings position NCDN and their associated dysregulated proteins as drivers of metastatic progression in CRC.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

DISEASE(S): Colon Cancer

SUBMITTER: Ana Montero Calle  

LAB HEAD: Rodrigo Barderas

PROVIDER: PXD061002 | Pride | 2026-05-03

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
TMT_NCDN_F1_Split_1_091653.raw Raw
TMT_NCDN_F1_Split_2_091956.raw Raw
TMT_NCDN_F2_Split_1_092051.raw Raw
TMT_NCDN_F2_Split_2_092407.raw Raw
TMT_NCDN_F3_Split_1_092513.raw Raw
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