Evidence map›Paper›PMID 30857208›Full record

ArticleCancers2019

Heterogeneous Nuclear Ribonucleoproteins A1 and A2 Function in Telomerase-Dependent Maintenance of Telomeres.

Tong-Hong Wang, Chin-Chuan Chen, Yuan-Chao Hsiao, Yu-Han Lin, Wen-Chieh Pi, Pei-Rong Huang, Tzu-Chien V Wang, Chi-Yuan Chen

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. 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

8 authors at 2 institutions in 1 country.

Tong-Hong WangGraduate Institute of Health Industry Technology and Research Center for Food and Cosmetic Safety, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Tao-Yuan 333, Taiwan. cellww@gmail.com.ORCID 0000-0001-9248-9031
Chin-Chuan ChenTissue Bank, Chang Gung Memorial Hospital, Linkou, Tao-Yuan 333, Taiwan. chinchuan@mail.cgu.edu.tw.
Yuan-Chao HsiaoDepartment of Molecular and Cellular Biology, College of Medicine, Chang Gung University, Tao-Yuan 333, Taiwan. c11kkh@gmail.com.
Yu-Han LinGraduate Institute of Health Industry Technology and Research Center for Food and Cosmetic Safety, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Tao-Yuan 333, Taiwan. evalin012880@gmail.com.
Wen-Chieh PiDepartment of Molecular and Cellular Biology, College of Medicine, Chang Gung University, Tao-Yuan 333, Taiwan. gratuit777@gmail.com.
Pei-Rong HuangDepartment of Molecular and Cellular Biology, College of Medicine, Chang Gung University, Tao-Yuan 333, Taiwan. telomerase0701@gmail.com.
Tzu-Chien V WangDepartment of Molecular and Cellular Biology, College of Medicine, Chang Gung University, Tao-Yuan 333, Taiwan. tcvwg@mail.cgu.edu.tw.
Chi-Yuan ChenGraduate Institute of Health Industry Technology and Research Center for Food and Cosmetic Safety, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Tao-Yuan 333, Taiwan. d49417002@gmail.com.
Chang Gung University of Science and Technology · TWChang Gung University · TW

Funding

Chang Gung Memorial Hospital; Ministry of Science and Technology, Taiwan CMRPD1F0452; CMRPF1G0121; MOST 106-2320-B-255-006-
6 · The paper itself

Abstract

The A/B subfamily of heterogeneous nuclear ribonucleoproteins (hnRNPs A/B), which includes hnRNP A1, A2/B1, and A3, plays an important role in cell proliferation. The simultaneous suppression of hnRNP A1/A2, but not the suppression of hnRNP A1 or A2 alone, has been shown to inhibit cell proliferation and induce apoptosis in cancer cells, but not in mortal normal cells. However, the molecular basis for such a differential inhibition of cell proliferation remains unknown. Here, we show that the simultaneous suppression of hnRNP A1 and hnRNP A2 resulted in dysfunctional telomeres and induced DNA damage responses in cancer cells. The inhibition of apoptosis did not alleviate the inhibition of cell proliferation nor the formation of dysfunctional telomeres in cancer cells depleted of hnRNP A1/A2. Moreover, while proliferation of mortal normal fibroblasts was not sensitive to the depletion of hnRNP A1/A2, the ectopic expression of hTERT in normal fibroblasts rendered these cells sensitive to proliferation inhibition, which was associated with the production of dysfunctional telomeres. Our study demonstrates that hnRNP A1 and A2 function to maintain telomeres in telomerase-expressing cells only, suggesting that the maintenance of functional telomeres in telomerase-expressing cancer cells employs factors that differ from those used in the telomerase-negative normal cells.

Indexed as

apoptosisDNA damage responseshnRNP A1/A2telomerasetelomeres

Identifiers

PMID30857208
PMCPMC6468650
OpenAlexW2920473389

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.