Evidence map›Paper›PMID 32476052›Full record

ArticlePharmaceutical research2020

Melanoma Cancer Immunotherapy Using PD-L1 siRNA and Imatinib Promotes Cancer-Immunity Cycle.

Chenyang Li, Xiuping Han

Abstract read
PubMed Publisher
In one paragraph

Article in Pharmaceutical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
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  4. Gene Therapies in Dermatological Diseases: A Breakthrough in Treatment.International journal of molecular sciences · 2025
    Review
  5. Recent Advances in Cancer Immunotherapy Aided by Regulatory Non-Coding RNA: A Review.Asian Pacific journal of cancer prevention : APJCP · 2025
    Review
  6. Review
  7. Article
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  13. RNA in Cancer Immunotherapy: Unlocking the Potential of the Immune System.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Review
  14. Review
  15. Article
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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

2 authors at 1 institution in 1 country.

Chenyang LiDepartment of Dermatology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China.
Xiuping HanDepartment of Dermatology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China. LiCY1470721@163.com.
China Medical University · CN

Funding

Shengjing Hospital of China Medical University, Shenyang -
6 · The paper itself

Abstract

purposeCancer-Immunity Cycle is a cascade of anticancer immune responses in the body that continues and fights against the cancer expansion. The Cancer-Immunity Cycle is halted by tumor cell immunosuppression of host T cell through programmed cell death receptor 1 (PD-1) and programmed cell death ligand 1 (PD-L1) interactions that induce the functional suppression of tumor-reactive cytotoxic T cells and actively promotes the tumorigenesis via the mTOR signaling pathway.

methodsHere, we demonstrated that this Cycle could be enhanced by the synergistic knock down of PD-L1 through co-delivery of siRNA-PD-L1 (siPD-L1) and imatinib (IMT) in a liposomal nanoparticle.

resultsThe siPDIN effectively downregulated the protein expressions of PD-L1 and significantly knocked down the expression of p-S6k protein at in vitro and in vivo conditions which inhibited tumorigenic mTOR pathway. The combination-based siPDIN exhibited a significantly higher cytotoxic effect compared to that of individual anticancer agents. B16F10 cells treated with siPDIN exhibited a significantly higher cancer cell apoptosis (~60%) compared to cocktail combination of siRNA+IMT (~35%) analyzed by flow cytometer. Importantly, siPDIN significantly delayed the tumor growth with significantly lower tumor-specific growth rate than the animals treated with individual free IMT or siRNA. siPDIN produced a 3-fold higher IFN-γ compared to control in DLNs and 4-fold higher IFN-γ in spleens.

conclusionOverall, results revealed that the tumors treated with siPDIN restored the immunity of CTLs by potentially inhibiting the immune checkpoint interactions, suppressed the mTOR signaling pathway and exhibited an enhanced anticancer efficacy in melanoma.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsB7-H1 AntigenCell Line, TumorDrug LiberationGene Expression Regulation, NeoplasticHumansImatinib MesylateInterferon-gammaLiposomesMelanoma, ExperimentalMiceNanoparticlesRNA, Small InterferingSkin NeoplasmsT-Lymphocytes, CytotoxicB7-H1 AntigenCd274 protein, mouseIFNG protein, mouseImatinib MesylateInterferon-gammaLiposomesRNA, Small Interferingimatinibimmune checkpoint inhibitorimmune responseliposomal nanoparticlesmelanomaPD-L1

Identifiers

PMID32476052
OpenAlexW3029995235

What OpenQuestion holds

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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.