Evidence map›Paper›PMID 29423000›Full record

ArticleAmerican journal of translational research2018

Silencing long noncoding RNA PVT1 inhibits tumorigenesis and cisplatin resistance of colorectal cancer.

Guanfang Ping, Wancheng Xiong, Lanfang Zhang, Yanru Li, Yusong Zhang, Yongli Zhao

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.0field-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

53 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  7. lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022
    Review
  8. Long non-coding RNA PVT1 facilitates cell migration and invasion by regulating miR-148a-3p and ROCK1 in breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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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

6 authors at 2 institutions in 1 country.

Guanfang PingDepartment of Pharmacy, The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100, Henan, China.
Wancheng XiongDepartment of General Surgery, The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100, Henan, China.
Lanfang ZhangDepartment of Digestive Internal Medicine, The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100, Henan, China.
Yanru LiDepartment of Intensive Care Unit, The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100, Henan, China.
Yusong ZhangDepartment of Pathology, Henan Cancer HospitalZhengzhou 450008, Henan, China.
Yongli ZhaoInterventional Section, The First Affiliated Hospital of Xinxiang Medical UniversityWeihui 453100, Henan, China.
First Affiliated Hospital of Xinxiang Medical University · CNHenan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) plays pivotal roles in tumorigenesis of many cancers, including colorectal cancer (CRC). However, the clinical significance and the biological functions of PVT1 in CRC remain largely unknown. In this study, we found that PVT1 was highly expressed in CRC tissues and cell lines compared with the corresponding non-cancerous samples and normal colon epithelial cells. Clinically, increased expression of PVT1 was positively correlated with tumor size, advanced histological stages, metastases, poor prognosis, and cisplatin resistance of CRC patients. In vitro studies showed that PVT1 silencing inhibited the proliferation, migration, invasion, and apoptosis escape of CRC cells. Knockdown of PVT1 in cisplatin-resistant CRC cells induced proliferation inhibition and apoptosis, whereas overexpression of PVT1 increased proliferation and decreased apoptosis of CRC cells. Mechanically, the levels of drug resistance-associated molecules, including multidrug resistance 1 and multidrug resistance protein 1, as well as the expression of anti-apoptotic Bcl-2 were significantly downregulated whereas the levels of pro-apoptotic Bax and cleaved caspase-3 were increased in PVT1-silenced cisplatin-resistant CRC cells. However, ectopic expression of PVT1 in CRC cells reversed the expressions of the molecules mentioned above. In addition, PVT1 overexpression in CRC cells significantly promoted cisplatin resistance in vivo. Collectively, these results demonstrated that PVT1 is a significant regulator in tumorigenesis and cisplatin resistance of CRC and provided evidence that PVT1 may be a promising target for CRC therapy.

Indexed as

cisplatin resistancecolorectal cancerPVT1tumorigenesis

Identifiers

PMID29423000
PMCPMC5801353
OpenAlexW3001713434

What OpenQuestion holds

Textmetadata
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.