Evidence map›Paper›PMID 31354026›Full record

ArticleChannels (Austin, Tex.)2019

Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage.

Li Liu, Yumei Chen, Qingyuan Zhang, Changzhong Li

Open access · goldAbstract read
In one paragraph

Article in Channels (Austin, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Ion Channels and Personalized Medicine in Gynecological Cancers.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  16. Review
  17. A Meta-Analysis Study to Infer Voltage-Gated KAntioxidants (Basel, Switzerland) · 2023
    Article
  18. Review
  19. From Channels to Canonical Wnt Signaling: A Pathological Perspective.International journal of molecular sciences · 2021
    Review
  20. Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020
    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

4 authors at 2 institutions in 1 country.

Li Liua Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , China.
Yumei Chenb Department of Obstetrics and Gynecology, Wenzhou People's Hospital , Wenzhou , Zhejiang , China.
Qingyuan Zhangc Department of Neurology, Wenzhou People's Hospital , Wenzhou , Zhejiang , China.
Changzhong Lia Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong University , Jinan , Shandong , China.
Shandong Provincial Hospital · CNWenzhou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1) is an important component of type A potassium channels, which has been found to be involved in various tumors. This study aimed to identify the role of KCNA1 in cervical cancer and explore the related mechanism. The levels of KCNA1 in cervical cancer tissues and cell lines were examined by Western blot and qPCR. Cell proliferation and invasion were assessed by CCK-8 and transwell assays, respectively. Protein levels of Hedgehog (Hhg), Wnt and Notch were detected by Western blot. The mitochondrial capacity was examined by immunostaining with MitoTracker Red CMXRos. KCNA1 was highly expressed in cervical cancer tissues and cell lines, and correlated with poor prognosis. In addition, depletion of KCNA1 suppressed growth, proliferation, migration and invasion of HeLa cells. Moreover, KCNA1 could regulate the Hhg, Wnt and Notch signaling pathways and cause mitochondrial dysfunction. The present study has demonstrated that KCNA1 is an oncogene excessively expressed in cervical cancer, and promotes tumor progression by regulating the Hhg, Wnt and Notch signaling pathways and the mitochondrial capacity. Therefore, our results provide a theoretical basis for the discovery of novel clinical treatment against cervical cancer.

Indexed as

Gene SilencingAnimalsCell Line, TumorCell MovementCell ProliferationFemaleHedgehogsHeLa CellsHumansKv1.1 Potassium ChannelMiceMice, Inbred NODMice, SCIDMitochondriaSignal TransductionUterine Cervical NeoplasmsKCNA1 protein, humanKv1.1 Potassium Channelcervical cancerHedgehog (Hhg)Notch signaling pathwayVoltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1)Wnt

Identifiers

PMID31354026
PMCPMC6682364
OpenAlexW2965702860

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.