ArticleCancers2021
Comparative Analysis of Stk11/Lkb1 versus Pten Deficiency in Lung Adenocarcinoma Induced by CRISPR/Cas9.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Age-associated B cells enhance tertiary lymphoid structures in the liver and promote HCC formation.Hepatology communications · 2025Article
- Dual-tracer autoradiographic analysis of glucose metabolism and hypoxia in orthotopic and PDX tumor models.Acta oncologica (Stockholm, Sweden) · 2025Article
- CRISPR/Cas9 model of prostate cancer identifies Kmt2c deficiency as a metastatic driver by Odam/Cabs1 gene cluster expression.Nature communications · 2024Article
- CRISPRingCancers · 2024Review
- The double-edge sword of CRISPR application forOncotarget · 2023Article
- Pre-Clinical Models to Study Human Prostate Cancer.Cancers · 2023Review
- Application of CRISPR for In Vivo Mouse Cancer Studies.Cancers · 2022Review
- Article
- AAV5 delivery of CRISPR-Cas9 supports effective genome editing in mouse lung airway.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- CRISPR and KRAS: a match yet to be made.Journal of biomedical science · 2021Review
- Targeting AP-1 transcription factors by CRISPR in the prostate.Oncotarget · 2021Article
- The CRISPR/Cas9 Minipig-A Transgenic Minipig to Produce Specific Mutations in Designated Tissues.Cancers · 2021Article
- LKB1 Regulates Goat Intramuscular Adipogenesis Through Focal Adhesion Pathway.Frontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
This study focused on STK11, PTEN, KRAS, and TP53, which are often found to be mutated in lung cancer. We compared Stk11 and Pten implication in lung cancer in combination with loss of Trp53 and gain of function of Kras in a CRISPR/Cas9 mouse model. Mice with loss of Stk11, Trp53, and KrasG12D mutation (SKT) reached human endpoint at around four months post-initiation. In comparison, mice with loss of Pten, Trp53, and KrasG12D mutation (PKT) survived six months or longer post-initiation. Pathological examination revealed an increase in proliferation in SKT deficient lung epithelia compared to PKT. This difference was independent of Pten loss, indicating that loss of Pten is dispensable for cell proliferation in lung adenocarcinoma. Furthermore, tumors with loss of Stk11, Trp53, and KrasG12D mutation had a significantly higher progression rate, monitored by PET/MRI scanning, compared to mice with loss of Pten, Trp53, and KrasG12D mutation, revealing that mutations in Stk11 are essential for adenocarcinoma progression. Overall, by using the CRISPR/Cas9 mouse model of lung adenocarcinoma, we showed that mutations in Stk11 are a key driver, whereas loss of Pten is dispensable for adenocarcinoma progression.
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