Evidence map›Paper›PMID 29577663›Full record

ArticleCancer medicine2018

Inhibition of breast cancer cell growth by methyl pyropheophenylchlorin photodynamic therapy is mediated though endoplasmic reticulum stress-induced autophagy in vitro and vivo.

Jiang Zhu, Si Tian, Kai-Ting Li, Qing Chen, Yuan Jiang, Hai-Dan Lin, Le-Hua Yu, Ding-Qun Bai

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Endoplasmic reticulum stress targeted therapy for breast cancer.Cell communication and signaling : CCS · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 1 country.

Jiang ZhuDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Si TianDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Kai-Ting LiDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qing ChenDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yuan JiangDepartment of Rehabilitation, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hai-Dan LinDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Le-Hua YuDepartment of Rehabilitation, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ding-Qun BaiDepartment of Rehabilitation, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0002-6727-4634
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNDalian Medical University · CNSouthwest University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy and ER stress participated in the inhibition of MPPa-PDT on tumor growth, but the molecular links between them remain undefined. We just explore the molecular mechanism between them in vitro and vivo. CCK-8 assay and flow cytometer were used to detect the cytotoxicity and mode of cell death after MPPa-PDT. Furthermore, the role of autophagy was verified in MPPa-PDT. Confocal microscopy was used to show the intracellular distribution of MPPa. ER stress markers and PERK signaling pathway were detected by western blot. While in vivo, tumor histology and immunohistochemistry were performed to show the effect of MPPa-PDT in mice. After MPPa-PDT, cells viability decreased in dose-dependent manner. Besides, the cell apoptosis increased along with the increasing of Beclin-1and LC3B II but declining of P62. When pretreated with 3-MA, LC3B II formation and the cytotoxicity declined. MPPa-PDT caused increasing of ER stress markers (GRP78, CHOP) as MPPa accumulated in ER. However, pretreatment with ER stress inhibitor 4PBA, the expression of GRP78 and LC3B II was blocked but the PERK signaling pathway activated and the expression of P62 increased. In vivo, the tumor growth was significantly inhibited by MPPa-PDT. Besides, the appearance of ER stress and autophagy was further demonstrated by immunohistochemistry. Our findings demonstrate that autophagy mediated by MPPa-PDT was regulated by ER stress, via PERK signaling pathway, to kill MDA-MB-231 cells in vitro and vivo.

Indexed as

AnimalsAutophagyBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivaleIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFemaleGene Expression Regulation, NeoplasticHumansMicePhotochemotherapyPorphyrinsSignal TransductionEIF2AK3 protein, humaneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanHspa5 protein, mousePorphyrinspyropheophorbide-a methylesterAutophagyendoplasmic reticulum stressmethyl pyropheophenylchlorinphotodynamic therapy

Identifiers

PMID29577663
PMCPMC5943539
OpenAlexW2790245884

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.