Evidence map›Paper›PMID 37122692›Full record

ArticleFrontiers in immunology2023

Melittin derived peptide-drug conjugate, M-DM1, inhibits tumor progression and induces effector cell infiltration in melanoma by targeting M2 tumor-associated macrophages.

Chanmi Jeong, Jeongdong Kim, Ik-Hwan Han, Soyoung Kim, Ilseob Choi, Hongsung Kim, Jin-Hyun Jeong, Hyunsu Bae

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.9field-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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  10. Melittin kills A549 cells by targeting mitochondria and blocking mitophagy flux.Redox report : communications in free radical research · 2023
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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

8 authors at 2 institutions in 1 country.

Chanmi JeongDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Jeongdong KimTwinpig Biolab Inc. Research & Development Center, Seoul, Republic of Korea.
Ik-Hwan HanDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Soyoung KimDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Ilseob ChoiDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Hongsung KimDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Jin-Hyun JeongCollege of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Incheon, Republic of Korea.
Hyunsu BaeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Kyung Hee University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Melanoma has the highest mortality rate among all the types of skin cancer. In melanoma, M2-like tumor-associated macrophages (TAMs) are associated with the invasiveness of tumor cells and a poor prognosis. Hence, the depletion or reduction of M2-TAMs is a therapeutic strategy for the inhibition of tumor progression. The aim of this study was to evaluate the therapeutic effects of M-DM1, which is a conjugation of melittin (M), as a carrier for M2-like TAMs, and mertansine (DM1), as a payload to induce apoptosis of TAMs, in a mouse model of melanoma. Methods: Melittin and DM1 were conjugated and examined for the characterization of M-DM1 by high-performance liquid chromatography and electrospray ionization mass spectrometry. Synthesized M-DM1 were examined for Results: M-DM1 was found to specifically reduce M2-like TAMs in melanoma, which potentially leads to the suppression of tumor growth, migration, and invasion. In addition, we also found that M-DM1 improved the survival rates in a mouse model of melanoma compared to M or DM1 treatment alone. Flow cytometric analysis revealed that M-DM1 enhanced the infiltration of CD8+ cytotoxic T cells and natural killer cells (NK cells) in the tumor microenvironment. Conclusion: Taken together, our findings highlight that M-DM1 is a prospective agent with enhanced anti-tumor effects.

Indexed as

MelanomaMelittenAnimalsFemaleMacrophagesMiceMice, Inbred C57BLProspective StudiesTumor-Associated MacrophagesTumor MicroenvironmentMelittenmelanomamelittinmertansinepeptide-drug conjugatetumor associated macrophages

Identifiers

PMID37122692
PMCPMC10140360
OpenAlexW4365516138

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.