Evidence map›Paper›PMID 26418750›Full record

ArticleOncotarget2015

Colorectal cancer-related mutant KRAS alleles function as positive regulators of autophagy.

Sara Alves, Lisandra Castro, Maria Sofia Fernandes, Rita Francisco, Paula Castro, Muriel Priault, Susana Rodrigues Chaves, Mary Pat Moyer, Carla Oliveira, Raquel Seruca and 3 more

Open 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. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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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 at 4 institutions in 3 countries.

Sara AlvesCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Lisandra CastroCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Maria Sofia FernandesIPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Rita FranciscoCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Paula CastroCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Muriel PriaultCNRS, UMR5095, University de Bordeaux 2, Bordeaux, France.
Susana Rodrigues ChavesCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Mary Pat MoyerINCELL Corporation, San Antonio, Texas, USA.
Carla OliveiraIPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Raquel SerucaIPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Manuela Côrte-RealCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Maria João SousaCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
Ana PretoCBMA - Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.
University of Minho · PTi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTIncell Corporation (United States) · USUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent interest to modulate autophagy in cancer therapy has been hampered by the dual roles of this conserved catabolic process in cancer, highlighting the need for tailored approaches. Since RAS isoforms have been implicated in autophagy regulation and mutation of the KRAS oncogene is highly frequent in colorectal cancer (CRC), we questioned whether/how mutant KRAS alleles regulate autophagy in CRC and its implications. We established two original models, KRAS-humanized yeast and KRAS-non-cancer colon cells and showed that expression of mutated KRAS up-regulates starvation-induced autophagy in both. Accordingly, KRAS down-regulation inhibited autophagy in CRC-derived cells harboring KRAS mutations. We further show that KRAS-induced autophagy proceeds via up-regulation of the MEK/ERK pathway in both colon models and that KRAS and autophagy contribute to CRC cell survival during starvation. Since KRAS inhibitors have proven difficult to develop, our results suggest using autophagy inhibitors as a combined/alternative therapeutic approach in CRCs with mutant KRAS.

Indexed as

AllelesMutationAutophagyBiomarkers, TumorCell SurvivalColorectal NeoplasmsExtracellular Signal-Regulated MAP KinasesGenotypeHCT116 CellsHumansMitogen-Activated Protein Kinase KinasesPhenotypeProto-Oncogene Proteins p21(ras)RNA InterferenceSaccharomyces cerevisiaeSignal TransductionBiomarkers, TumorExtracellular Signal-Regulated MAP KinasesKRAS protein, humanMitogen-Activated Protein Kinase KinasesProto-Oncogene Proteins p21(ras)autophagycolorectal cancerhumanized yeastKRAS mutationsnon-cancer colon cells

Identifiers

PMID26418750
PMCPMC4741568
OpenAlexW1946100424

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.