Evidence map›Paper›PMID 31942696›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2020

STAT3 inhibitory stattic enhances immunogenic cell death induced by chemotherapy in cancer cells.

Sevda Jafari, Afsaneh Lavasanifar, Mohammad Saied Hejazi, Nasrin Maleki-Dizaji, Mehran Mesgari, Ommoleila Molavi

Open access · greenAbstract read
In one paragraph

Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-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

31 citing papers in PubMed, 52 citations in OpenAlex.

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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 2 institutions in 2 countries.

Sevda JafariBiotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Afsaneh LavasanifarFaculty of Pharmacy and Pharmaceutical Science, University of Alberta, Edmonton, Canada.
Mohammad Saied HejaziDepartment of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
Nasrin Maleki-DizajiDepartment of Pharmacology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehran MesgariDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ommoleila MolaviBiotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. omolavi@ualberta.ca.ORCID http://orcid.org/0000-0002-1820-7048
Tabriz University of Medical Sciences · IRUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInduction of immunogenic cell death (ICD) is considered a promising strategy for cancer immunotherapy. Stattic is an inhibitor of STAT3, which is found constitutively active in many cancers and plays a major role in cancer progression.

objectivesIn the present study, we proposed to evaluate whether stattic can enhance the effects of chemotherapy in the induction of ICD in cancer cells harboring hyperactive STAT3.

methodsThe growth inhibitory effects of stattic and chemo agents including doxorubicin (DOX) and oxaliplatin (OXP) were evaluated using MTT assay in B16F10 and CT26 cell lines. Flow cytometry was applied to study cell apoptosis and calreticulin (CRT) surface exposure. The levels of high mobility group box 1 (HGMB1), heat shock protein70 (HSP70) and interleukin-12 (IL-12) were measured using ELISA.

resultsTreatment of B16F10 and CT26 cells with stattic in combination with DOX resulted in synergistic antitumor effects with combination index being 0.82 and 0.87, respectively. Interestingly, we found a higher level of ICD markers including CRT expression as well as HMGB1 and HSP70 secretion in the cells received combination therapy of stattic and DOX as compared with monotherapies. Moreover, exposure of dendritic cells (DCs) to conditioned media (CM) from cancer cells treated with stattic and/or DOX resulted in secretion of IL-12, which is an indicator of DCs maturation and induction of Th1 response. OXP and stattic monotherapy induced ICD in CT26 cells and stimulated IL-12 secretion by DCs; however, we did not observe a significant increase in the level of ICD in CT26 cells and IL-12 secretion by DCs when CT26 cells were treated with stattic and OXP combination as compared with monotherapy groups.

conclusionThese findings indicate that STAT3 inhibitory stattic can increase ICD induced by DOX. Graphical abstract.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCyclic S-OxidesDendritic CellsDoxorubicinHMGB1 ProteinHSP70 Heat-Shock ProteinsImmunogenic Cell DeathInterleukin-12Mice, Inbred C57BLNeoplasmsOxaliplatinSTAT3 Transcription FactorAntineoplastic AgentsCyclic S-OxidesDoxorubicinHMGB1 ProteinHMGB1 protein, mouseHSP70 Heat-Shock ProteinsInterleukin-12OxaliplatinStat3 protein, mouseSTAT3 Transcription FactorstatticChemotherapyColon cancerCombination therapyImmunotherapyMelanomaSTAT3

Identifiers

PMID31942696
PMCPMC7214602
OpenAlexW2999224494

What OpenQuestion holds

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Registered trials

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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.