Evidence map›Paper›PMID 31637011›Full record

ArticleSignal transduction and targeted therapy

E6-induced selective translation of WNT4 and JIP2 promotes the progression of cervical cancer via a noncanonical WNT signaling pathway.

Lin Zhao, Longlong Wang, Chenglan Zhang, Ze Liu, Yongjun Piao, Jie Yan, Rong Xiang, Yuanqing Yao, Yi Shi

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Cancers · 2023
    Article
  10. The Roles of Secreted Wnt Ligands in Cancer.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. miR-4721, Induced by EBV-miR-BART22, TargetsMolecular therapy. Nucleic acids · 2020
    Article
  19. Review
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 1 institution in 1 country.

Lin Zhao1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Longlong Wang1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Chenglan Zhang1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Ze Liu1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Yongjun Piao1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.ORCID 0000-0002-2769-6437
Jie Yan1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Rong Xiang1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Yuanqing Yao1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.
Yi Shi1School of Medicine, Nankai University, 94 Weijin Road, 300071 Tianjin, China.ORCID 0000-0003-2530-410X
Nankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mRNA translation reprogramming occurs frequently in many pathologies, including cancer and viral infection. It remains largely unknown whether viral-induced alterations in mRNA translation contribute to carcinogenesis. Most cervical cancer is caused by high-risk human papillomavirus infection, resulting in the malignant transformation of normal epithelial cells mainly via viral E6 and E7 oncoproteins. Here, we utilized polysome profiling and deep RNA sequencing to systematically evaluate E6-regulated mRNA translation in HPV18-infected cervical cancer cells. We found that silencing E6 can cause over a two-fold change in the translation efficiency of ~653 mRNAs, most likely in an eIF4E- and eIF2α-independent manner. In addition, we identified that E6 can selectively upregulate the translation of WNT4, JIP1, and JIP2, resulting in the activation of the noncanonical WNT/PCP/JNK pathway to promote cell proliferation in vitro and tumor growth in vivo. Ectopic expression of WNT4/JIP2 can effectively rescue the decreased cell proliferation caused by E6 silencing, strongly suggesting that the WNT4/JIP2 pathway mediates the role of E6 in promoting cell proliferation. Thus, our results revealed a novel oncogenic mechanism of E6 via regulating the translation of mRNAs.

Indexed as

Cancer genomicsGynaecological cancer

Identifiers

PMID31637011
PMCPMC6799841
OpenAlexW2973085745

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.