Evidence map›Paper›PMID 31581233›Full record

ArticlePloS one2019

RPL22L1 induction in colorectal cancer is associated with poor prognosis and 5-FU resistance.

Shuyun Rao, Suraj Peri, Jens Hoffmann, Kathy Q Cai, Bryan Harris, Michele Rhodes, Denise C Connolly, Joseph R Testa, David L Wiest

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

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  8. Ribosome Structural Changes Dynamically Affect Ribosome Function.International journal of molecular sciences · 2024
    Review
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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

9 authors at 3 institutions in 2 countries.

Shuyun RaoCenter for Translational Medicine, Department of Surgery, George Washington University, Washington, DC, United States of America.
Suraj PeriBlood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
Jens HoffmannExperimental Pharmacology & Oncology Berlin-Buch GMBH, Berlin-Buch, Germany.
Kathy Q CaiCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
Bryan HarrisBlood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
Michele RhodesBlood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
Denise C ConnollyMolecular Therapeutics Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
Joseph R TestaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.
David L WiestBlood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA, United States of America.ORCID 0000-0002-0792-3188
Fox Chase Cancer Center · USGeorge Washington University · USHelios Hospital Berlin-Buch · DE

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
Basis for Lymphomagenesis in Akt2 Transgenic MiceR01CA077429 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TESTA, JOSEPH R. · 1998 to 2013
$4.7M
Regulation of Hematopoiesis by Ribosomal Protein ParalogsR01AI110985 · NIAID · RESEARCH INST OF FOX CHASE CAN CTR · PI WIEST, DAVID L. · 2015 to 2019
$2.0M
Rpl22-Like1 as a Novel Prognostic Marker in Colorectal CancerR21CA216825 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI WIEST, DAVID L. · 2018 to 2019
$432k
NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA077429NCI NIH HHS R21 CA216825NIAID NIH HHS R01 AI110985
6 · The paper itself

Abstract

We have previously demonstrated that loss of the tumor suppressive activity of ribosomal protein (RP) RPL22 predisposes to development of leukemia in mouse models and aggressive disease in human patients; however, the role of RPL22 in solid tumors, specifically colorectal cancer (CRC), had not been explored. We report here that RPL22 is either deleted or mutated in 36% of CRC and provide new insights into its mechanism of action. Indeed, Rpl22 inactivation causes the induction of its highly homologous paralog, RPL22L1, which serves as a driver of cell proliferation and anchorage-independent growth in CRC cells. Moreover, RPL22L1 protein is highly expressed in patient CRC samples and correlates with poor survival. Interestingly, the association of high RPL22L1 expression with poor prognosis appears to be linked to resistance to 5-Fluorouracil, which is a core component of most CRC therapeutic regimens. Indeed, in an avatar trial, we found that human CRC samples that were unresponsive to 5-Fluorouracil in patient-derived xenografts exhibited elevated expression levels of RPL22L1. This link between RPL22L1 induction and 5-Fluorouracil resistance appears to be causal, because ectopic expression or knockdown of RPL22L1 in cell lines increases and decreases 5-Fluorouracil resistance, respectively, and this is associated with changes in expression of the DNA-repair genes, MGMT and MLH1. In summary, our data suggest that RPL22L1 might be a prognostic marker in CRC and predict 5-FU responsiveness.

Indexed as

Drug Resistance, NeoplasmAnimalsCell ProliferationColorectal NeoplasmsDNA Modification MethylasesDNA Repair EnzymesFluorouracilHumansMiceMutL Protein Homolog 1PrognosisProto-Oncogene ProteinsRibosomal ProteinsRNA-Binding ProteinsTumor Suppressor ProteinsDNA Modification MethylasesDNA Repair EnzymesFluorouracilMGMT protein, humanMLH1 protein, humanMutL Protein Homolog 1Proto-Oncogene ProteinsRibosomal ProteinsRNA-Binding ProteinsRPL22L1 protein, humanRPL22L1 protein, mouseRPL22 protein, humanTumor Suppressor Proteins

Identifiers

PMID31581233
PMCPMC6776433
OpenAlexW2979076895

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.