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STK11

STK11

Overview

STK11 encodes serine/threonine kinase 11, also known as LKB1, a protein kinase with broad roles in cellular energy sensing, polarity, and growth control. It is a key upstream regulator of the AMPK pathway and related signaling networks, including downstream effects on mTOR-associated metabolism and stress responses. Because of these functions, STK11 is biologically important in maintaining normal cellular homeostasis and is frequently studied in cancer biology as a tumor suppressor-associated target.

In biomedical research, STK11 is especially relevant in contexts where altered metabolic signaling intersects with immune regulation and therapy response. Recent studies have examined STK11 in relation to checkpoint inhibitor, anti-PD-1 therapy, PD-L1-linked immune escape, and oncogenic KRAS-mutant disease, particularly non-small cell lung cancer and triple-negative breast cancer. These studies reinforce STK11’s role as a signaling node connecting metabolism, tumor proliferation, and antitumor immunity.

Recent Publications Focus

Below is a summary of the newest research publications targeting STK11 (sorted by publication date).

  • PMID: 42406708 (2026-07-06) — In a colorectal cancer liver metastasis cohort treated with anti-EGFR-based conversion chemotherapy, next-generation resequencing identified recurrent STK11 mutations among additional resistance-associated alterations. The study reported STK11 in 20.6% of post-treatment samples, supporting its appearance as part of the mutational landscape observed after therapy and suggesting a possible role in anti-EGFR resistance biology.

  • PMID: 42048614 (2026-07-02) — This study examined STK11-mutant lung adenocarcinoma and found that tumor-derived complement C3 overexpression promoted tumor growth and immune checkpoint inhibitor resistance. The authors noted that loss-of-function STK11 mutations occur in 15% to 20% of lung adenocarcinomas and correlate with immunotherapy failure and worse survival. The work links STK11 deficiency to immune evasion and highlights complement signaling as a downstream feature of the STK11-mutant tumor state.

  • PMID: 42285688 (2026-07-01) — In a psoriasis-focused study, Yinxie Granules were reported to act through the STING/NF-κB pathway to reduce cutaneous inflammation and vasculopathy. The publication specifically stated that the treatment had no significant impact on upstream regulators including TRAF6, LKB1, AMPK, and ULK1. Although STK11 itself was not the direct therapeutic target, LKB1 was included among the upstream signaling components assessed in the pathway analysis.

  • PMID: 42377736 (2026-06-30) — This clinical outcomes study evaluated metastatic non-small cell lung cancer and compared tumors with single STK11 mutations against those with co-occurring KEAP1 and Kras mutations. The report emphasized that these mutation patterns commonly occur in mNSCLC, reinforcing the importance of STK11 in molecular stratification of advanced lung cancer and in understanding combined oncogenic and tumor-suppressive pathway disruption.

  • PMID: 42162294 (2026-06-01) — In ovarian cancer, inhibition of salt-inducible kinases reprogrammed T cells and enhanced antitumor immunity. The study noted that human T cells in patient ascites express high levels of SIK and the upstream kinase LKB1, and that SIK inhibition strongly activated antitumor responses. This places STK11/LKB1 upstream of immune-cell metabolic control in a tumor microenvironment context.

  • PMID: 42061410 (2026-04-29) — This mechanistic study on prexasertib showed that its cytotoxic effect results from dual inhibition of CHK1 and AMPK. The authors reported increased AMPKα Thr172 phosphorylation via CAMKK2 and LKB1, indicating that STK11/LKB1 participates in the signaling axis affected by the drug. The work connects STK11-related AMPK activation to pharmacologic response.

  • PMID: 42018410 (2026-04-28) — The study focused on STK11-mutant NSCLC and showed that targeting CRTC2 reversed tumor resistance to immunotherapy. It stated that patients with tumors harboring STK11 mutations are resistant to standard-of-care anti-PD-1/PD-L1 blockade. This publication reinforces the central role of STK11 loss in immune checkpoint resistance and suggests CRTC2 as a downstream vulnerability.

  • PMID: 41966774 (2026-04-10) — In triple-negative breast cancer, celastrol was reported to inhibit immune escape and proliferation through the LKB1-AMPK-PD-L1/MYC signaling pathway. The study explored regulatory mechanisms underlying celastrol’s antitumor effects and proposed this axis as a potential therapeutic target. Here, STK11/LKB1 is positioned as a key upstream regulator of AMPK-linked immune and proliferative signaling.

  • PMID: 41634944 (2026-02-03) — This study assessed first-line immunochemotherapy outcomes across Kras mutation subtypes in advanced lung adenocarcinoma. STK11 co-mutations were enriched in Kras G12C, Kras G12V, and other subtypes, and they correlated with shorter progression-free survival. The findings support the clinical relevance of STK11 status when interpreting Kras-driven disease and treatment response.

Overall, these recent publications portray STK11 as a central tumor suppressor and signaling regulator whose loss or pathway perturbation is repeatedly associated with poor outcomes, immune resistance, and altered response to targeted therapy or immunotherapy. Across lung adenocarcinoma, metastatic NSCLC, colorectal cancer metastases, ovarian cancer, psoriasis-related signaling, and triple-negative breast cancer, STK11/LKB1 appears in contexts involving AMPK, CAMKK2, CRTC2, PD-L1, STING-NF-κB, Kras, and checkpoint blockade, underscoring its broad biomedical significance.

Background PMIDs

  • [PMID 42048614]

Method PMIDs

  • [PMID 42048614]
  • [PMID 42061410]

Target PMIDs

  • [PMID 42285688]
  • [PMID 42377736]
  • [PMID 41966774]
  • [PMID 41634944]
  • [PMID 42162294]
  • [PMID 42018410]
  • [PMID 42406708]
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