Evidence map›Paper›PMID 39906392›Full record

ArticleFrontiers in pharmacology2024

Tanshinlactone triggers methuosis in breast cancer cells via NRF2 activation.

Wanjun Lin, Zifeng Huang, Xuening Zhang, Dayuan Zheng, Yanchao Yang, Meina Shi, Dongfang Yang, Tong Chu, Wenzhe Ma

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Wanjun LinState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Zifeng HuangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Xuening ZhangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Dayuan ZhengState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Yanchao YangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Meina ShiState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Dongfang YangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Tong ChuState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Wenzhe MaState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Tanshinlactone is a compound derived from the herb Methods: The effect of tanshinlactone on the growth of human cancer cells was evaluated using sulforhodamine B and colony formation assay. Fluorescent dyes are used to label macropinosomes and lysosomes. Phase contrast, confocal and transmission electron microscopy were employed to observe cell morphological changes. RT-PCR, western blot, lentiviral-mediated gene overexpression, and pharmacological inhibitor assays were comprehensively designed to regulate the identified signaling pathways and confirm the mechanism of tanshinlactone. Human breast cancer cell lines-derived xenograft tumor explants assay was used to evaluate the compound's efficacy and to assess the induction of methuosis via NRF2 activation by tanshinlactone. Results: Tanshinlactone selectively inhibits the growth of ER+ and HER2+/EGFR + breast cancer cells while showing limited cytotoxicity against other cancer types and normal cells. The selective anti-breast cancer activity is associated with the induction of methuosis, characterized by cytoplasmic vacuolization due to dysfunctional macropinocytosis. This process is mediated by the activation of the transcription factor NRF2, leading to the formation of macropinosomes that fail to fuse with lysosomes or recycle to the plasma membrane, resulting in cell death. The Conclusion: Tanshinlactone as a novel therapeutic agent, is capable of selectively inhibiting ER+ and HER2+/EGFR + breast tumors through a unique mechanism of inducing catastrophic macropinocytosis. This regimen holds promise for targeted therapy with minimized side effects and offers a new therapeutic avenue for breast patients with drug-resistant diseases.

Indexed as

breast cancercatastrophic macropinocytosisdrug resistancemethuosisNRF2 activationtanshinlactone

Identifiers

PMID39906392
PMCPMC11790599

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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.