Evidence map›Paper›PMID 38132099›Full record

ArticleCells2023

RL2 Enhances the Elimination of Breast Cancer Cells by Doxorubicin.

Fabian Wohlfromm, Kamil Seyrek, Nikita Ivanisenko, Olga Troitskaya, Dagmar Kulms, Vladimir Richter, Olga Koval, Inna N Lavrik

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026
    Review
  3. Review
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 3 institutions in 2 countries.

Fabian WohlfrommTranslational Inflammation Research, Medical Faculty, Center of Dynamic Systems (CDS), Otto von Guericke University, 39120 Magdeburg, Germany.
Kamil SeyrekTranslational Inflammation Research, Medical Faculty, Center of Dynamic Systems (CDS), Otto von Guericke University, 39120 Magdeburg, Germany.
Nikita IvanisenkoTranslational Inflammation Research, Medical Faculty, Center of Dynamic Systems (CDS), Otto von Guericke University, 39120 Magdeburg, Germany.
Olga TroitskayaTranslational Inflammation Research, Medical Faculty, Center of Dynamic Systems (CDS), Otto von Guericke University, 39120 Magdeburg, Germany.ORCID 0000-0003-2902-7656
Dagmar KulmsExperimental Dermatology, Department of Dermatology, TU-Dresden, 01307 Dresden, Germany.
Vladimir RichterDepartment of Biotechnology, Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences (SB RAS), 630090 Novosibirsk, Russia.
Olga KovalDepartment of Biotechnology, Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences (SB RAS), 630090 Novosibirsk, Russia.ORCID 0000-0001-7788-2249
Inna N LavrikTranslational Inflammation Research, Medical Faculty, Center of Dynamic Systems (CDS), Otto von Guericke University, 39120 Magdeburg, Germany.
Otto-von-Guericke-Universität Magdeburg · DEInstitute of Chemical Biology and Fundamental Medicine · RUNational Center for Tumor Diseases · DE

Funding

Deutsche Forschungsgemeinschaft LA2386
6 · The paper itself

Abstract

RL2 (recombinant lactaptin 2), a recombinant analogon of the human milk protein Κ-Casein, induces mitophagy and cell death in breast carcinoma cells. Furthermore, RL2 was shown to enhance extrinsic apoptosis upon long-term treatment while inhibiting it upon short-term stimulation. However, the effects of RL2 on the action of chemotherapeutic drugs that induce the intrinsic apoptotic pathway have not been investigated to date. Here, we examined the effects of RL2 on the doxorubicin (DXR)-induced cell death in breast cancer cells with three different backgrounds. In particular, we used BT549 and MDA-MB-231 triple-negative breast cancer (TNBC) cells, T47D estrogen receptor alpha (ERα) positive cells, and SKBR3 human epidermal growth factor receptor 2 (HER2) positive cells. BT549, MDA-MB-231, and T47D cells showed a severe loss of cell viability upon RL2 treatment, accompanied by the induction of mitophagy. Furthermore, BT549, MDA-MB-231, and T47D cells could be sensitized towards DXR treatment with RL2, as evidenced by loss of cell viability. In contrast, SKBR3 cells showed almost no RL2-induced loss of cell viability when treated with RL2 alone, and RL2 did not sensitize SKBR3 cells towards DXR-mediated loss of cell viability. Bioinformatic analysis of gene expression showed an enrichment of genes controlling metabolism in SKBR3 cells compared to the other cell lines. This suggests that the metabolic status of the cells is important for their sensitivity to RL2. Taken together, we have shown that RL2 can enhance the intrinsic apoptotic pathway in TNBC and ERα-positive breast cancer cells, paving the way for the development of novel therapeutic strategies.

Indexed as

Triple Negative Breast NeoplasmsApoptosisCell Line, TumorDoxorubicinEstrogen Receptor alphaHumansDoxorubicinEstrogen Receptor alphabreast cancerDXRintrinsic cell deathlactaptinmitophagyRL2Κ-Casein

Identifiers

PMID38132099
PMCPMC10741759
OpenAlexW4389399379

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.