Evidence map›Paper›PMID 34771150›Full record

ArticleMolecules (Basel, Switzerland)2021

Chloroquine Potentiates the Anticancer Effect of Pterostilbene on Pancreatic Cancer by Inhibiting Autophagy and Downregulating the RAGE/STAT3 Pathway.

Rong-Jane Chen, Yi-Jhen Lyu, Yu-Ying Chen, Yen-Chien Lee, Min-Hsiung Pan, Yuan-Soon Ho, Ying-Jan Wang

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2021. 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
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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Stilbenes from Vine Extracts: Therapeutic Potential and Mechanisms.International journal of molecular sciences · 2025
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  11. The role of autophagy in pancreatic diseases.Frontiers in pharmacology · 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

7 authors at 5 institutions in 1 country.

Rong-Jane ChenDepartment of Food Safety/Hygiene and Risk Management, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan.ORCID 0000-0002-2326-934X
Yi-Jhen LyuDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan.
Yu-Ying ChenDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan.
Yen-Chien LeeDepartment of Medical Oncology, Tainan Hospital, Ministry of Health and Welfare, Executive Yuan, Tainan 70043, Taiwan.
Min-Hsiung PanInstitute of Food Science and Technology, National Taiwan University, Taipei 10617, Taiwan.ORCID 0000-0002-5188-7030
Yuan-Soon HoTMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0002-3649-6680
Ying-Jan WangDepartment of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan 70403, Taiwan.ORCID 0000-0003-3169-2495
National Cheng Kung University · TWChest Hospital, Ministry of Health and Welfare · TWKaohsiung Medical University · TWNational Taiwan University · TWTaipei Medical University Hospital · TW

Funding

Ministry of Science and Technology, Taiwan MOST 106-2314-B-006-029-MY3Ministry of Science and Technology, Taiwan MOST 107-2311-B-006 -004 -MY3Ministry of Science and Technology, Taiwan MOST 109-2314-B-006 -051 -MY3
6 · The paper itself

Abstract

The treatment of pancreatic ductal adenocarcinoma (PDAC) remains a huge challenge, because pro-survival signaling pathways-such as the receptor for advanced glycation end products (RAGE)/signal transducer and activator of transcription 3 (STAT3) pathway-are overexpressed in PDAC cells. Moreover, PDAC cells are highly resistant to chemotherapeutic agents because of autophagy induction. Therefore, autophagy and its modulated signaling pathways are attractive targets for developing novel therapeutic strategies for PDAC. Pterostilbene is a stilbenoid chemically related to resveratrol, and has potential for the treatment of cancers. Accordingly, we investigated whether the autophagy inhibitor chloroquine could potentiate the anticancer effect of pterostilbene in the PDAC cell lines MIA PaCa-2 and BxPC-3, as well as in an orthotopic animal model. The results indicated that pterostilbene combined with chloroquine significantly inhibited autophagy, decreased cell viability, and sensitized the cells to pterostilbene-induced apoptosis via downregulation of the RAGE/STAT3 and protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways in PDAC cells. The results of the orthotopic animal model showed that pterostilbene combined with chloroquine significantly inhibited pancreatic cancer growth, delayed tumor quadrupling times, and inhibited autophagy and STAT3 in pancreatic tumors. In summary, the present study suggested the novel therapeutic strategy of pterostilbene combined with chloroquine against the growth of pancreatic ductal adenocarcinoma by inhibiting autophagy and downregulating the RAGE/STAT3 signaling pathways.

Indexed as

Antigens, NeoplasmAntineoplastic AgentsAutophagyCarcinoma, Pancreatic DuctalCell ProliferationCells, CulturedCell SurvivalChloroquineDown-RegulationDrug Screening Assays, AntitumorHumansMitogen-Activated Protein KinasesPancreatic NeoplasmsSTAT3 Transcription FactorStilbenesAntigens, NeoplasmAntineoplastic AgentsChloroquineMitogen-Activated Protein KinasesMOK protein, humanpterostilbeneSTAT3 protein, humanSTAT3 Transcription FactorStilbenesapoptosisautophagychloroquinepancreatic ductal adenocarcinomapterostilbeneRAGE/STAT3

Identifiers

PMID34771150
PMCPMC8588513
OpenAlexW3212423331

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.