Evidence map›Paper›PMID 34072621›Full record

ArticleCancers2021

Ubiquitin Specific Protease 29 Functions as an Oncogene Promoting Tumorigenesis in Colorectal Carcinoma.

Arun Pandian Chandrasekaran, Bharathi Suresh, Neha Sarodaya, Na-Re Ko, Seung-Jun Oh, Kye-Seong Kim, Suresh Ramakrishna

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  13. Dual role of deubiquitinating enzyme USP19 regulates mitotic progression and tumorigenesis by stabilizing survivin.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  14. 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

7 authors at 2 institutions in 1 country.

Arun Pandian ChandrasekaranDepartment of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong, Seoul 04763, Korea.ORCID 0000-0003-2358-7345
Bharathi SureshDepartment of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong, Seoul 04763, Korea.
Neha SarodayaDepartment of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong, Seoul 04763, Korea.
Na-Re KoBiomedical Research Center, Asan Institute for Life Sciences, Seoul 05505, Korea.ORCID 0000-0003-0726-1783
Seung-Jun OhAsan Medical Center, Department of Nuclear Medicine, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa, Seoul 05505, Korea.ORCID 0000-0002-3769-067X
Kye-Seong KimDepartment of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong, Seoul 04763, Korea.
Suresh RamakrishnaDepartment of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-ro, Seongdong, Seoul 04763, Korea.
Hanyang University · KRUlsan College · KR

Funding

Korea Health Industry Development Institute HI18C2383National Research Foundation of Korea 2017M3A9B3061830National Research Foundation of Korea 2018M3A9H3022412
6 · The paper itself

Abstract

Colorectal carcinoma is the third foremost cause of cancer-related deaths and accounts for 5.8% of all deaths globally. The molecular mechanisms of colon cancer progression and metastasis control are not well studied. Ubiquitin-specific protease 29 (USP29), a deubiquitinating enzyme, is involved in the occurrence and development of wide variety of cancers. However, its clinical significance and biological roles in colorectal carcinoma (CRC) remain unexplored. In this research, we observed that the rate of USP29 overexpression was higher in colon cancer patient tissues relative to its corresponding normal tissues. CRISPR-Cas9-mediated depletion of USP29 triggered DNA double strand breaks and delayed cell-cycle progression in HCT116 cells. We also demonstrated that USP29 depletion hampers the colony formation and increases apoptosis of HCT116 cells. USP29 knockdown significantly decreased CRC cell proliferation in vitro. Depletion of USP29 in HCT116 cells substantially reduced the tumor volume of mouse xenografts. In conclusion, our study shows that elevated expression of USP29 promotes malignancy in CRC, suggesting that USP29 could be a promising target for colon cancer therapy.

Indexed as

colorectal carcinomaCRISPR-Cas9deubiquitinating enzymesDNA damagemouse modelsoncogenesisubiquitin specific protease

Identifiers

PMID34072621
PMCPMC8197902
OpenAlexW3165490994

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.