Evidence map›Paper›PMID 29024940›Full record

ArticleBritish journal of cancer2017

ANO9/TMEM16J promotes tumourigenesis via EGFR and is a novel therapeutic target for pancreatic cancer.

Ikhyun Jun, Hyung Soon Park, He Piao, Jung Woo Han, Min Ji An, Byeong Gyu Yun, Xianglan Zhang, Yong Hoon Cha, You Keun Shin, Jong In Yook and 6 more

Abstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Anoctamin 9 determines CaFrontiers in immunology · 2025
    Article
  8. Article
  9. TMEM16 proteins: CaInternational journal of molecular medicine · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. CaInternational journal of molecular sciences · 2022
    Article
  19. Review
  20. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    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

16 authors.

Ikhyun JunDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Hyung Soon ParkDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
He PiaoDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Jung Woo HanDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Min Ji AnDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Byeong Gyu YunDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Xianglan ZhangOral Cancer Research Institute, Yonsei University College of Dentistry, Seoul 03722, Korea.
Yong Hoon ChaDepartment of Oral Pathology, Oral Cancer Institute, Yonsei University College of Dentistry, Seoul 03722, Korea.
You Keun ShinDivision of Medical Oncology, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, 211, Eonju-Ro, Gangnam-Gu, Seoul, 06273, Korea.
Jong In YookDepartment of Oral Pathology, Oral Cancer Institute, Yonsei University College of Dentistry, Seoul 03722, Korea.
Jinsei JungDepartment of Otorhinolaryngology, Yonsei University College of Medicine, Seoul 03722, Korea.
Heon Yung GeeDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.
Joon Seong ParkDepartment of Surgery, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06273, Korea.
Dong Sup YoonDepartment of Surgery, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06273, Korea.
Hei-Cheul JeungDivision of Medical Oncology, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, 211, Eonju-Ro, Gangnam-Gu, Seoul, 06273, Korea.
Min Goo LeeDepartment of Pharmacology and Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, 50-1, Yonsei-Ro, Seodaemun-Gu, Seoul 03722, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnoctamin (ANO)/transmembrane member 16 (TMEM16) proteins mediate diverse physiological and pathophysiological functions including cancer cell proliferation. The present study aimed to identify the role of ANOs in pancreatic cancer.

methodsIn an initial screen of ANOs, ANO9/TMEM16J was overexpressed in pancreatic cancer cells, and its role in the pathogenesis of pancreatic cancer was evaluated using an integrated in vitro and in vivo approach. To determine clinical relevance of the experimental findings, the prognostic value of ANO9 was evaluated in patients with pancreatic cancer.

resultsThe ANO9 mRNA and protein levels were increased in pancreatic cancer-derived cells. Exogenous expression of ANO9 in PANC-1 cells significantly increased cell proliferation in cell cultures and in mice. In contrast, knockdown of ANO9 in AsPC-1, BxPC-3, and Capan-2 cells strongly inhibited cell proliferation. Mechanistic analysis suggested that physical association of ANO9 with epidermal growth factor receptor (EGFR) underlies ANO9-induced cell proliferation. Knockdown of ANO9 augmented the effects of the EGFR inhibitor and the cytotoxic agent on pancreatic cancer cell proliferation. In addition, high ANO9 expression is a poor prognostic factor in patients with pancreatic cancer.

conclusionsThe ANO9/TMEM16J appears to be a clinically useful prognostic marker for pancreatic cancer and a potential therapeutic target.

Indexed as

AdultAgedAged, 80 and overAnimalsAnoctaminsAnti-Bacterial AgentsAntineoplastic AgentsBiomarkers, TumorCarcinogenesisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationDeoxycytidineDisease-Free SurvivalDoxycyclineErbB ReceptorsANO9 protein, humanAno9 protein, mouseAnoctaminsAnti-Bacterial AgentsAntineoplastic AgentsBiomarkers, TumorDeoxycytidineDoxycyclineErbB ReceptorsErlotinib HydrochlorideGemcitabineMembrane ProteinsPhospholipid Transfer ProteinsRNA, Messenger

Identifiers

PMID29024940
PMCPMC5729472

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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.