Target intelligence / Profile preview

Proline-rich mitotic checkpoint control factor (PRCC)

Target
PRCC
Molecular classification
Other (pre-mRNA splicing factor-related), Other (mitotic checkpoint-associated protein)
01

Overview

Proline-rich mitotic checkpoint control factor (PRCC) is a ubiquitously expressed, proline-rich human protein encoded by the PRCC gene. PRCC interacts with the mitotic checkpoint protein MAD2B (also called MAD2L2 or hRev7), which implicates it in the regulation of the spindle assembly checkpoint and mitotic progression[1][3]. In papillary renal cell carcinoma (RCC), recurrent chromosomal translocations t(X;1)(p11;q21) generate oncogenic gene fusions between PRCC and the transcription factor TFE3, resulting in the PRCC-TFE3 chimeric protein[1][2][3][5]. This fusion protein alters gene transactivation, disrupts cell cycle checkpoint functions, and confers a growth advantage to tumor cells. The presence of PRCC-TFE3 rearrangements serves as a diagnostic marker for a specific molecular subtype of papillary RCC[2]. No direct drugs target PRCC, but the PRCC-TFE3 fusion’s disruption of normal mitotic checkpoint control is fundamental to its oncogenicity. Key points: - PRCC is a mitotic checkpoint control protein and possible splicing factor[1][2][5]. - The oncogenic PRCC-TFE3 fusion protein is crucial in specific papillary renal cell carcinomas[1][2][3][5]. - No drugs or direct inhibitors are currently identified for PRCC; its primary disease relevance is as a fusion oncogene and cancer biomarker[2][3]. - PRCC is not classified as a classical receptor, enzyme, transporter, or ion channel, but rather as an “other” class protein with cell cycle and splicing roles.

Other names
Proline-rich protein PRCCPRCCTPRCRCCP1Papillary renal cell carcinoma translocation-associated gene proteinPapillary renal cell carcinoma (translocation-associated)PRCC-TFE3 fusion protein
02

Mechanism of action

None established for direct targeting; PRCC-TFE3 fusion may contribute to oncogenesis via dominant-negative effects on mitotic checkpoint (interaction with MAD2B) and altered transcriptional activity[1][2][3][5].

03

Biological functions

Cell cycleMitotic checkpoint controlPre-mRNA splicing
04

Disease associations

Cancer, specifically papillary renal cell carcinoma (translocation-associated)
05

Safety considerations

No notable direct therapeutic safety concerns reportedfusions may disrupt cell cycle checkpoints
06

Biomarkers

PRCC-TFE3 fusion (positive by FISH) for diagnosis of a specific subtype of papillary renal cell carcinoma[2]

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