Evidence map›Paper›PMID 29749475›Full record

ArticleInternational journal of oncology2018

miR-125a induces apoptosis, metabolism disorder and migrationimpairment in pancreatic cancer cells by targeting Mfn2-related mitochondrial fission.

Lichao Pan, Lin Zhou, Weijia Yin, Jia Bai, Rong Liu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Lichao PanThe Second Department of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Lin ZhouDepartment of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Weijia YinDepartment of Biochemistry, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Jia BaiDepartment of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Rong LiuThe Second Department of Hepatobiliary Surgery, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial fission is important for the development and progression of pancreatic cancer (PC). However, little is known regarding its role in pancreatic cancer apoptosis, metabolism and migration. In the current study, the mechanism by which mitochondrial fission modifies the biological characteristics of PC was explored. MicroRNA‑125a (miR‑125a) had the ability to inhibit mitochondrial fission and contributed to cellular survival. Suppressed mitochondrial fission led to a reduction in mitochondrial debris, preserved the mitochondrial membrane potential, inhibited mitochondrial permeability transition pore opening, ablated cytochrome c leakage into the cytoplasm and reduced the pro‑apoptotic protein contents, finally blocking mitochondria related apoptosis pathways. Furthermore, defective mitochondrial fission induced by miR‑125a enhanced mitochondria‑dependent energy metabolism by promoting activity of electron transport chain complexes. Furthermore, suppressed mitochondrial fission also contributed to PANC‑1 cell migration by preserving the F‑actin balance. Furthermore, mitofusin 2 (Mfn2), the key defender of mitochondrial fission, is involved in inhibition of miR125a‑mediated mitochondrial fission. Low contents of miR‑125a upregulated Mfn2 transcription and expression, leading to inactivation of mitochondrial fission. Ultimately, the current study determined that miR‑125a and Mfn2 are regulated by hypoxia‑inducible factor 1 (HIF1). Knockdown of HIF1 reversed miR‑125a expression, and therefore, inhibited Mfn2 expression, leading to activation of mitochondrial fission. Collectively, the present study demonstrated mitochondrial fission as a tumor suppression process that is regulated by the HIF/miR‑125a/Mfn2 pathways, acting to restrict PANC‑1 cell survival, energy metabolism and migration, with potential implications for novel approaches for PC therapy.

Indexed as

AdenoviridaeAnimalsApoptosisCell Line, TumorCell MovementCell SurvivalEnergy MetabolismGene Expression Regulation, NeoplasticGenetic VectorsGTP PhosphohydrolasesHumansHypoxia-Inducible Factor 1, alpha SubunitMembrane Potential, MitochondrialMiceMicroRNAsMitochondrial DynamicsGTP PhosphohydrolasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMFN2 protein, humanMicroRNAsMIRN125 microRNA, humanMitochondrial Proteins

Identifiers

PMID29749475
PMCPMC5958665
OpenAlexW2801701541

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.