Evidence map›Paper›PMID 25704884›Full record

ArticleOncotarget2015

Autophagy induction by leptin contributes to suppression of apoptosis in cancer cells and xenograft model: involvement of p53/FoxO3A axis.

Saroj Nepal, Mi Jin Kim, Jin Tae Hong, Sang Hyun Kim, Dong-Hwan Sohn, Sung Hee Lee, Kyung Song, Dong Young Choi, Eung Seok Lee, Pil-Hoon Park

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
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

46 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  5. Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024
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  12. Obesity: a perfect storm for carcinogenesis.Cancer metastasis reviews · 2022
    Review
  13. Obesity and Breast Cancer Risk: The Oncogenic Implications of Metabolic Dysregulation.The Journal of clinical endocrinology and metabolism · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Saroj NepalCollege of Pharmacy, Yeungnam University, Gyeongsangbuk-do, Republic of Korea.
Mi Jin KimCollege of Pharmacy, Yeungnam University, Gyeongsangbuk-do, Republic of Korea.
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.
Sang Hyun KimDepartment of Pharmacology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
Dong-Hwan SohnInstitute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Sung Hee LeeInstitute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Kyung SongInstitute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Dong Young ChoiCollege of Pharmacy, Yeungnam University, Gyeongsangbuk-do, Republic of Korea.
Eung Seok LeeCollege of Pharmacy, Yeungnam University, Gyeongsangbuk-do, Republic of Korea.
Pil-Hoon ParkCollege of Pharmacy, Yeungnam University, Gyeongsangbuk-do, Republic of Korea.
Yeungnam University · KRWonkwang University · KRChungbuk National University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leptin, a hormone mainly produced from adipose tissue, has been shown to induce proliferation of cancer cells. However, the molecular mechanisms underlying leptin-induced tumor progression have not been clearly elucidated. In the present study, we investigated the role of autophagy in leptin-induced cancer cell proliferation using human hepatoma (HepG2) and breast cancer cells (MCF-7), and tumor growth in a xenograft model. Herein, we showed that leptin treatment caused autophagy induction as assessed by increase in expression of autophagy-related genes, including beclin-1, Atg5 and LC3 II, further induction of autophagosome formation and autophagic flux. Interestingly, inhibition of autophagic process by treatment with inhibitors and LC3B gene silencing blocked leptin-induced increase in cell number and suppression of apoptosis, indicating a crucial role of autophagy in leptin-induced tumor progression. Moreover, gene silencing of p53 or FoxO3A prevented leptin-induced LC3 II protein expression, suggesting an involvement of p53/FoxO3A axis in leptin-induced autophagy activation. Leptin administration also accelerated tumor growth in BALB/c nude mice, which was found to be autophagy dependent. Taken together, our results demonstrate that leptin-induced tumor growth is mediated by autophagy induction and autophagic process would be a promising target to regulate development of cancer caused by leptin production.

Indexed as

ApoptosisAnimalsApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein 5bcl-2-Associated X ProteinBeclin-1Disease ProgressionForkhead Box Protein O3Forkhead Transcription FactorsGene SilencingGenes, p53Hep G2 CellsHumansLeptinMaleApoptosis Regulatory ProteinsATG5 protein, humanAutophagy-Related Protein 5BAX protein, humanbcl-2-Associated X ProteinBeclin-1BECN1 protein, humanForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanLeptinMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated ProteinsTP53 protein, humanTumor Suppressor Protein p53apoptosisautophagyFoxO3Aleptinp53

Identifiers

PMID25704884
PMCPMC4466676
OpenAlexW1571499367

What OpenQuestion 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 OpenQuestion graph.