Evidence map›Paper›PMID 36765853›Full record

ArticleCancers2023

Exosome-Transmitted tRF-16-K8J7K1B Promotes Tamoxifen Resistance by Reducing Drug-Induced Cell Apoptosis in Breast Cancer.

Chunxiao Sun, Xiang Huang, Jun Li, Ziyi Fu, Yijia Hua, Tianyu Zeng, Yaozhou He, Ningjun Duan, Fan Yang, Yan Liang and 4 more

Abstract read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

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

20 citing papers in PubMed.

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  20. International journal of biological sciences · 2024
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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

14 authors.

Chunxiao SunDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiang HuangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.ORCID 0000-0002-7448-1711
Jun LiDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Ziyi FuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yijia HuaDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Tianyu ZengDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yaozhou HeDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Ningjun DuanDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Fan YangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yan LiangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.ORCID 0000-0002-6972-2541
Hao WuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Wei LiDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yuchen ZhangThe First Clinical College, Nanjing Medical University, Nanjing 210029, China.
Yongmei YinDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.ORCID 0000-0003-3335-369X

Funding

National Natural Science Foundation of China 81902704、81972484
6 · The paper itself

Abstract

Tamoxifen resistance remains a challenge in hormone receptor-positive (HR+) breast cancer. Recent evidence suggests that transfer ribonucleic acid (tRNA)-derived fragments play pivotal roles in the occurrence and development of various tumors. However, the relationship between tRNA-derived fragments and tamoxifen resistance remains unclear. In this study, we found that the expression of tRF-16-K8J7K1B was upregulated in tamoxifen-resistant cells in comparison with tamoxifen-sensitive cells. Higher levels of tRF-16-K8J7K1B were associated with shorter disease-free survival in HR+ breast cancer. Overexpression of tRF-16-K8J7K1B promotes tamoxifen resistance. Moreover, extracellular tRF-16-K8J7K1B could be packaged into exosomes and could disseminate tamoxifen resistance to recipient cells. Mechanistically, exosomal tRF-16-K8J7K1B downregulates the expression of apoptosis-related proteins, such as caspase 3 and poly (ADP-ribose) polymerase, by targeting tumor necrosis factor-related apoptosis-inducing ligand in receptor cells, thereby reducing drug-induced cell apoptosis. Therapeutically, the inhibition of exosomal tRF-16-K8J7K1B increases the sensitivity of breast cancer cells to tamoxifen in vivo. These data demonstrate that exosomal tRF-16-K8J7K1B may be a novel therapeutic target to overcome tamoxifen resistance in HR+ breast cancer.

Indexed as

breast cancerexosomestamoxifen resistancetRNA-derived fragments

Identifiers

PMID36765853
PMCPMC9913720

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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.