Evidence map›Paper›PMID 41408407›Full record

ArticleExperimental & molecular medicine2025

ULK1 knockout suppresses pancreatic cancer progression by inhibiting autophagy and enhancing antitumor immunity.

Hana Jeong, Jinju Lee, Ji-Yoon Son, JinKyung Lee, Miju Kang, Sunghyeon Cho, Ji Hyeon Kim, Yoon Jeon, Jonghyun Lee, Dongkwan Shin and 3 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Hana Jeong *Cancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Jinju Lee *Cancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Ji-Yoon Son *Cancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
JinKyung LeeCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Miju KangCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Sunghyeon ChoCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Ji Hyeon KimCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Yoon JeonCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Jonghyun LeeBioinformatics Branch, Division of Cancer Data Science, Research Institute, National Cancer Center, Goyang, Republic of Korea.
Dongkwan ShinBioinformatics Branch, Division of Cancer Data Science, Research Institute, National Cancer Center, Goyang, Republic of Korea.ORCID http://orcid.org/0000-0002-6925-1081
Hye-Ran KimCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea.
Ho LeeDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang, Republic of Korea.ORCID http://orcid.org/0000-0001-5573-742X
Heesun CheongCancer Metastasis Branch, Division of Cancer Biology, Research Institute National Cancer Center, Goyang, Republic of Korea. heesunch@ncc.re.kr.ORCID http://orcid.org/0000-0003-1946-107X

Funding

National Cancer Center (NCC) NCC-24H1200National Cancer Center (NCC) NCC-2510750National Cancer Center (NCC) NCC_2510750National Research Foundation of Korea (NRF) 2020R1A2B5B01002011
6 · The paper itself

Abstract

Autophagy plays a dual role in cancer, acting as a tumor suppressor and promoter depending on tumor stage and context. While Atg5 and Atg7 are well established core autophagy genes, the role of Unc-51-like kinase 1 (ULK1)-a key autophagy initiator-remains poorly understood in pancreatic ductal adenocarcinoma (PDAC). Here we investigated the role of ULK1 using tissue-specific deletion in genetically engineered mouse models. Although ULK1 messenger RNA levels remained unchanged between normal and tumor cells in The Cancer Genome Atlas dataset, multiplex immunohistochemistry revealed elevated ULK1 activity, marked by pATG14, in high-grade human PDAC tissues. Genetic deletion of Ulk1 impaired autophagy and reduced cell proliferation, colony formation and invasiveness of pancreatic cancer cells. In vivo, both syngeneic orthotopic and KPC (LSL-Kras

Indexed as

AutophagyAutophagy-Related Protein-1 HomologCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalDisease ProgressionHumansIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutTumor MicroenvironmentAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsULK1 protein, humanUlk1 protein, mouse

Identifiers

PMID41408407
PMCPMC12800254

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.