Evidence map›Paper›PMID 30478628›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2019

KIAA1199 promotes invasion and migration in non-small-cell lung cancer (NSCLC) via PI3K-Akt mediated EMT.

Zhiyuan Tang, Yang Ding, Qin Shen, Caixin Zhang, Jun Li, Mohammed Nazar, Yan Wang, Xiaoyu Zhou, Jianfei Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The crucial role of CEMIP in cancer metastasis: Mechanistic insights and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

9 authors at 3 institutions in 1 country.

Zhiyuan TangDepartment of Clinical Biobank, Nantong University Affiliated Hospital, Nantong, 226001, Jiangsu, China.
Yang DingState Key Laboratory of Natural Medicines, Department of Pharmaceutics, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, 210009, China.
Qin ShenDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Caixin ZhangDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Jun LiDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Mohammed NazarDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Yan WangDepartment of Emergency Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Xiaoyu ZhouDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. hx730303@163.com.
Jianfei HuangDepartment of Clinical Biobank, Nantong University Affiliated Hospital, Nantong, 226001, Jiangsu, China. jfhuang@ntu.edu.cn.
Affiliated Hospital of Nantong University · CNNantong University · CNChina Pharmaceutical University · CN

Funding

Key Technology Research of Nantong-People's Livelihood MS22015114Six Talent Peaks Project in Jiangsu Province 2015- WSW-049Young Scientists Fund 81503143
6 · The paper itself

Abstract

KIAA1199 is often upregulated in cancer cells, including non-small-cell lung cancer (NSCLC). Although KIAA1199 is associated with aggressive tumor phenotype and poor survival in NSCLC, little is known about its functional role in NSCLC progression. Using archived clinical samples, we evaluated KIAA1199 messenger RNA (mRNA) and protein expression in NSCLC tissues and correlated with NSCLC clinicopathological characteristics as well as overall survival. Using NSCLC cell lines, KIAA1199 was either silenced using gene-specific shRNA or overexpressed to assess the impact on EMT signaling pathways. Finally, in a mouse xenograft NSCLC model, we determine the therapeutic potential of KIAA1199 repression. Our data showed that KIAA1199 was significantly upregulated in NSCLC tissues compared to adjacent normal tissues both at the mRNA (P < 0.001) and protein levels (P < 0.05). KIAA1199 overexpression is an independent prognostic marker for overall survival (HR = 1.833). In NSCLC cell lines, KIAA1199 expression directly influences the expression of EMT markers, EMT-inducing transcription factors (EMT-TFs), and EMT signaling molecules. Knocking down of KIAA1199 expression in the mouse NSCLC xenograft model significantly suppressed tumor growth and augmented the efficacy of chemotherapy (n = 5; P < 0.05). We conclude that KIAA1199 is not only a prognostic marker but a novel therapeutic target in NSCLC through regulating EMT signaling pathway. KEY MESSAGES: KIAA1199 overexpression is an independent prognostic marker in NSCLC. KIAA1199 expression directly influences the expression of EMT markers. KIAA1199 promotes invasion and migration in NSCLC via PI3K-Akt mediated EMT.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansHyaluronoglucosaminidaseLung NeoplasmsMaleMiceMice, NudeMiddle AgedNeoplasm InvasivenessPhosphatidylinositol 3-KinasesCEMIP protein, humanCemip protein, mouseHyaluronoglucosaminidasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktKIAA1199MetastasisNSCLC

Identifiers

PMID30478628
OpenAlexW2903092053

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.