Evidence map›Paper›PMID 30046371›Full record

ArticleOxidative medicine and cellular longevity2018

Mitofusin2 Induces Cell Autophagy of Pancreatic Cancer through Inhibiting the PI3K/Akt/mTOR Signaling Pathway.

Ran Xue, Qinghua Meng, Di Lu, Xinjuan Liu, Yanbin Wang, Jianyu Hao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

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  7. Role of Sphingosine-1-Phosphate Signaling Pathway in Pancreatic Diseases.International journal of molecular sciences · 2024
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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

6 authors at 1 institution in 1 country.

Ran XueDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Qinghua MengDepartment of Critical Care Medicine of Liver Disease, Beijing You-An Hospital, Capital Medical University, Beijing 100069, China.ORCID 0000-0001-9967-6403
Di LuDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0001-7322-5495
Xinjuan LiuDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0001-5817-6699
Yanbin WangDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0002-4331-3192
Jianyu HaoDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0001-7881-9380
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimPancreatic cancer is one of the most quickly fatal cancers around the world. Burgeoning researches have begun to prove that mitochondria play a crucial role in cancer treatment. Mitofusin2 (Mfn2) plays an indispensable role in mitochondrial fusion and adjusting function. However, the role and underlying mechanisms of Mfn2 on cell autophagy of pancreatic cancer is still unclear. Our aim was to explore the effect of Mfn2 on multiple biological functions involving cell autophagy in pancreatic cancer.

methodsPancreatic cancer cell line, Aspc-1, was treated with Ad-Mfn2 overexpression. Western blotting, caspase-3 activity measurement, and CCK-8 and reactive oxygen species (ROS) assay were used to examine the effects of Mfn2 on pancreatic cancer autophagy, apoptosis, cell proliferation, oxidative stress, and PI3K/Akt/mTOR signaling. The expression of tissue Mfn2 was detected by immunohistochemical staining. Survival analysis of Mfn2 was evaluated by OncoLnc.

resultsMfn2 improved the expression of LC3-II and Bax and downregulated the expression of P62 and Bcl-2 in pancreatic cancer cells. Meanwhile, Mfn2 also significantly inhibited the expression of p-PI3K, p-Akt, and p-mTOR proteins in pancreatic cancer cells. In addition, Mfn2 inhibited pancreatic cancer cell proliferation and ROS production. Assessment of Kaplan-Meier curves showed that Mfn2

conclusionsOur finding suggests that Mfn2 induces cell autophagy of pancreatic cancer through inhibiting the PI3K/Akt/mTOR signaling pathway. Meanwhile, Mfn2 also influences multiple biological functions of pancreatic cancer cells. Mfn2 may act as a therapeutic target in pancreatic cancer treatment.

Indexed as

ApoptosisAutophagyCell Line, TumorCell ProliferationGTP PhosphohydrolasesHumansMitochondrial ProteinsPancreatic NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionTOR Serine-Threonine KinasesGTP PhosphohydrolasesMFN2 protein, humanMitochondrial ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine Kinases

Identifiers

PMID30046371
PMCPMC6038474
OpenAlexW2811471450

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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.