Evidence map›Paper›PMID 36834940›Full record

ArticleInternational journal of molecular sciences2023

Inhibition of Ribosomal RNA Processing 15 Homolog (RRP15) Suppressed Tumor Growth, Invasion and Epithelial to Mesenchymal Transition (EMT) of Colon Cancer.

Zirong Deng, Yun Xu, Yuchen Cai, Weiling Lin, Libei Zhang, Aoqing Jiang, Yuhang Zhou, Rui Zhao, Heyan Zhao, Zhaoguo Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  2. Article
  3. Article
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

11 authors at 1 institution in 1 country.

Zirong DengDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.ORCID 0000-0002-8737-9337
Yun XuDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Yuchen CaiDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Weiling LinDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Libei ZhangDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Aoqing JiangDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Yuhang ZhouDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Rui ZhaoDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Heyan ZhaoDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Zhaoguo LiuDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.ORCID 0000-0001-6311-8338
Tingdong YanDepartment of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.ORCID 0000-0002-5193-022X
Nantong University · CN

Funding

China Postdoctoral Science Foundation 2018M642296Nantong Science and Technology Bureau JC2021024Nantong Science and Technology Bureau JC2021025National Natural Science Foundation of China 31972889National Natural Science Foundation of China 81703884
6 · The paper itself

Abstract

Although ribosomal RNA processing 15 Homolog (RRP15) has been implicated in the occurrence of various cancers and is considered a potential target for cancer treatment, its significance in colon cancer (CC) is unclear. Thus, this present study aims to determine RRP15 expression and biological function in CC. The results demonstrated a strong expression of RRP15 in CC compared to normal colon specimens, which was correlated with poorer overall survival (OS) and disease-free survival (DFS) of the patients. Among the nine investigated CC cell lines, RRP15 demonstrated the highest and lowest expression in HCT15 and HCT116 cells, respectively. In vitro assays demonstrated that the knockdown of RRP15 inhibited the growth, colony-forming ability and invasive ability of the CC cells whereas its overexpression enhanced the above oncogenic function. Moreover, subcutaneous tumors in nude mice showed that RRP15 knockdown inhibited the CC growth while its overexpression enhanced their growth. Additionally, the knockdown of RRP15 inhibited the epithelial-mesenchymal transition (EMT), whereas overexpression of RRP15 promoted the EMT process in CC. Collectively, inhibition of RRP15 suppressed tumor growth, invasion and EMT of CC, and might be considered a promising therapeutic target for treating CC.

Indexed as

Colonic NeoplasmsEpithelial-Mesenchymal TransitionRibosomal ProteinsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMice, NudeRNA Processing, Post-TranscriptionalRNA, RibosomalRibosomal ProteinsRNA, RibosomalRRP15 protein, humanRrp15 protein, mousecolon cancerepithelial-mesenchymal transitioninvasionribosomal RNA processing 15 Homologtumor growth

Identifiers

PMID36834940
PMCPMC9965612
OpenAlexW4319985575

What OpenQuestion holds

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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.