# INPPL1

Source: https://onco.cc/targets/inppl1/  
OnCo record `inppl1` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

INPPL1 (Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Endometrial cancer.

## Summary

Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyses the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways. Required for correct mitotic spindle orientation and therefore progression of mitosis. Plays a central role in regulation of PI3K-dependent insulin signalling, although the precise molecular mechanisms and signalling pathways remain unclear.

IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Endometrial Carcinoma.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: inositol polyphosphate phosphatase like 1; Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2; SHIP2
- Tags: cancer-genes-wave
- Symbol: INPPL1
- Class: tumor-suppressor
- Biology: Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyses the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways. Required for correct mitotic spindle orientation and therefore progression of mitosis. Plays a central role in regulation of PI3K-dependent insulin signalling, although the precise molecular mechanisms and signalling pathways remain unclear. While overexpression reduces both insulin-stimulated MAP kinase and Akt activation, its absence does not affect insulin signalling or GLUT4 trafficking. Confers resistance to dietary obesity. May act by regulating AKT2, but not AKT1, phosphorylation at the plasma membrane. Location: Cytoplasm, cytosol; Cytoplasm, cytoskeleton; Membrane; Cell projection, filopodium (UniProt). Locus 11q13.4 (HGNC).
- Where found: Endometrial cancer: IntOGen driver in 1 cohort (UCEC)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 1 cohort. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:6080: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:6080
- UniProt O15357: https://www.uniprot.org/uniprotkb/O15357/entry
- NCBI Gene 3636: https://www.ncbi.nlm.nih.gov/gene/3636
- Ensembl ENSG00000165458: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000165458

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/)
- cancers: [Endometrial cancer](https://onco.cc/cancers/endometrial/)

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JSON: https://onco.cc/api/v1/entities/inppl1.json