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Malignant peripheral nerve sheath tumor (MPNST) tumor samples

ABSTRACT: Malignant peripheral nerve sheath tumor (MPNST) is an aggressive sarcoma. Comprehensive proteomic profiles of 23 MPNST tumor specimens were obtained using LC-MS/MS. Among 23 tumor specimens, 13 patients showed favorable prognosis and 10 did local recurrence/distant metastasis.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Tadashi Kondo

PROVIDER: PXD030585 | JPOST Repository | Thu Dec 22 00:00:00 GMT 2022

REPOSITORIES: jPOST

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			Action	DRS
	MPNST_case1.raw	Raw
	MPNST_case10.raw	Raw
	MPNST_case11.raw	Raw
	MPNST_case12.raw	Raw
	MPNST_case13.raw	Raw

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Project description:Malignant nerve sheath tumors (MPNST) are rare types of malignant soft tissue sarcomas and characterized by high resistance for current chemotherapeutic strategies, including topoisomerase 2a (TOP2A) inhibitor, etoposide. Although the poor therapeutic or severe side effects of etoposide in MPNST patients are demonstrated, novel molecular targets that promote tumor malignancy have not been identified. Previously, we reported that paired related-homeobox 1 (PRRX1) serves as a malignant factor in human osteosarcoma. Here, we found that expression level of PRRX1 in tumor tissues, especially sarcomas, are higher than in normal tissues using database analysis. PRRX1 was expressed in various human sarcoma tissues, and its level increased during malignant progression from schwannoma or neurofibroma to MPNST. High expression of PRRX1 was also associated with poor prognosis of human MPNST patients, and PRRX1 knockdown suppressed proliferation, invasion and tumorigenic potential of human MPNST cell line, HS-PSS. Immunoprecipitation and mass spectrometry analysis revealed that PRRX1 interacts with TOP2A, and human MPNST patients with high expression of TOP2A showed poor prognosis. Interestingly, database analysis revealed that expression level of TOP2A in tumor tissues were positively correlated with PRRX1. TOP2A knockdown in HS-PSS suppressed proliferation, and inhibited the migration induced by PRRX1A overexpression. Overexpression of PRRX1 and TOP2A cooperatively increased migration and expression of tumor-malignancy associated gene sets, including EMT, mTORC1, KRAS and SRC signaling pathways. Inhibition of PRRX1-TOP2A interaction would be a novel tumor-selective therapeutic strategy that has less severe side effects than current chemotherapies.

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