# STK11

Source: https://onco.cc/targets/stk11/  
OnCo record `stk11` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

STK11 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response.

## Summary

Tumour suppressor serine/threonine-protein kinase that controls the activity of AMP-activated protein kinase (AMPK) family members, thereby playing a role in various processes such as cell metabolism, cell polarity, apoptosis and DNA damage response. Acts by phosphorylating the T-loop of AMPK family proteins, thus promoting their activity: phosphorylates PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2, MARK3, MARK4, NUAK1, NUAK2, SIK1, SIK2, SIK3 and SNRK but not MELK. Also phosphorylates non-AMPK family proteins such as STRADA, PTEN and possibly p53/TP53.

CIViC holds 23 clinical evidence items and 0 assertions across 8 variants, naming Sirolimus, MEK Inhibitor CI-1040, Everolimus and Cisplatin/Pembrolizumab/Pemetrexed Regimen and others. Open Targets scores its association with cancer at 0.87 (direct and indirect evidence; datatypes genetic literature 0.75, affected pathway 0.96, literature 1.00, genetic association 0.72, somatic mutation 0.96, animal model 0.77). IntOGen calls it a driver in 14 cohorts (3 activating, 11 loss-of-function), covering Anal Squamous Cell Carcinoma, Cervical Adenocarcinoma, Cervical Squamous Cell Carcinoma, Cholangiocarcinoma, Lung Adenocarcinoma, Non-Small Cell Lung Cancer and others.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: serine/threonine kinase 11; Serine/threonine-protein kinase STK11; LKB1
- Tags: cancer-genes-wave
- Symbol: STK11
- Class: kinase
- Biology: Tumour suppressor serine/threonine-protein kinase that controls the activity of AMP-activated protein kinase (AMPK) family members, thereby playing a role in various processes such as cell metabolism, cell polarity, apoptosis and DNA damage response. Acts by phosphorylating the T-loop of AMPK family proteins, thus promoting their activity: phosphorylates PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2, MARK3, MARK4, NUAK1, NUAK2, SIK1, SIK2, SIK3 and SNRK but not MELK. Also phosphorylates non-AMPK family proteins such as STRADA, PTEN and possibly p53/TP53. Acts as a key upstream regulator of AMPK by mediating phosphorylation and activation of AMPK catalytic subunits PRKAA1 and PRKAA2 and thereby regulates processes including: inhibition of signalling pathways that promote cell growth and proliferation when energy levels are low, glucose homeostasis in liver, activation of autophagy when cells undergo nutrient deprivation, and B-cell differentiation in the germinal centre in response to DNA damage. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton. Required for cortical neuron polarisation by mediating phosphorylation and activation of BRSK1 and BRSK2, leading to axon initiation and specification. Location: Nucleus; Cytoplasm; Membrane; Mitochondrion (UniProt). Locus 19p13.3 (HGNC).
- Where found: Lung cancer: Open Targets association 0.75 with lung cancer (MONDO_0008903); Ovarian cancer: Open Targets association 0.64 with ovarian cancer (MONDO_0008170); Cervical cancer: Open Targets association 0.61 with cervical cancer (MONDO_0002974); IntOGen driver in 3 cohorts (CEAD, CESC); Breast cancer: Open Targets association 0.54 with breast cancer (MONDO_0007254); CIViC evidence names this disease; Prostate cancer: CIViC evidence names this disease; Pancreatic ductal adenocarcinoma: CIViC evidence names this disease

## 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: CIViC lists 17 therapies; IntOGen calls it an activating (Act) driver in 3 cohorts; IntOGen calls it a loss-of-function (LoF) driver in 11 cohorts; CIViC holds 23 clinical evidence items on its variants; UniProt keyword "DNA damage". Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Diseases the sources name that have no OnCo cancer page yet, so they are not linked: Peutz-Jeghers Syndrome.

## Sources

- HGNC HGNC:11389: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:11389
- UniProt Q15831: https://www.uniprot.org/uniprotkb/Q15831/entry
- NCBI Gene 6794: https://www.ncbi.nlm.nih.gov/gene/6794
- Ensembl ENSG00000118046: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000118046

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Anal cancer (squamous cell carcinoma)](https://onco.cc/cancers/anal/), [Breast cancer (all types)](https://onco.cc/cancers/breast-cancer/), [Cervical cancer](https://onco.cc/cancers/cervical/), [Lung cancer (all types)](https://onco.cc/cancers/lung-cancer/), [Ovarian cancer](https://onco.cc/cancers/ovarian/), [Pancreatic ductal adenocarcinoma](https://onco.cc/cancers/pancreatic/), [Prostate cancer](https://onco.cc/cancers/prostate/), [Thyroid cancer](https://onco.cc/cancers/thyroid/)
- pathways: [KEAP1-NRF2 antioxidant pathway](https://onco.cc/pathways/keap1-nrf2/), [Lipid synthesis, uptake & cholesterol](https://onco.cc/pathways/lipid-metabolism-cancer/)
- trials: [A Study of JAB-21822 in Advanced or Metastatic NSCLC With KRAS p.G12C and STK11 Co-mutation and Wild-type KEAP1](https://onco.cc/trials/nct05276726/), [A Study to Investigate the Efficacy of Durvalumab Plus Tremelimumab in Combination With Chemotherapy Compared With Pembrolizumab in Combination With Chemotherapy in Metastatic NSCLC Patients With Non-squamous Histology Who Have Mutations and/or Co-mutations in STK11, KEAP1, or KRAS](https://onco.cc/trials/nct06008093/), [Study of Efficacy and Safety of JDQ443 Single-agent as First-line Treatment for Patients With Locally Advanced or Metastatic KRAS G12C- Mutated Non-small Cell Lung Cancer With a PD-L1 Expression < 1% or a PD-L1 Expression ≥ 1% and an STK11 Co-mutation.](https://onco.cc/trials/nct05445843/), [Study of TNG260 and an Anti-PD Antibody in STK11 Mutated Solid Tumors](https://onco.cc/trials/nct05887492/)

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JSON: https://onco.cc/api/v1/entities/stk11.json