Exosome-Transmitted tRF-16-K8J7K1B Promotes Tamoxifen Resistance by Reducing Drug-Induced Cell Apoptosis in Breast Cancer
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..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
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| Enthalten in: |
Cancers - 15(2023), 3, p 899 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Chunxiao Sun [VerfasserIn] |
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| Links: |
doi.org [kostenfrei] |
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| Themen: |
Breast cancer |
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| doi: |
10.3390/cancers15030899 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
DOAJ08067318X |
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| 520 | |a 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. | ||
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| 653 | 0 | |a Neoplasms. Tumors. Oncology. Including cancer and carcinogens | |
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| 700 | 0 | |a Jun Li |e verfasserin |4 aut | |
| 700 | 0 | |a Ziyi Fu |e verfasserin |4 aut | |
| 700 | 0 | |a Yijia Hua |e verfasserin |4 aut | |
| 700 | 0 | |a Tianyu Zeng |e verfasserin |4 aut | |
| 700 | 0 | |a Yaozhou He |e verfasserin |4 aut | |
| 700 | 0 | |a Ningjun Duan |e verfasserin |4 aut | |
| 700 | 0 | |a Fan Yang |e verfasserin |4 aut | |
| 700 | 0 | |a Yan Liang |e verfasserin |4 aut | |
| 700 | 0 | |a Hao Wu |e verfasserin |4 aut | |
| 700 | 0 | |a Wei Li |e verfasserin |4 aut | |
| 700 | 0 | |a Yuchen Zhang |e verfasserin |4 aut | |
| 700 | 0 | |a Yongmei Yin |e verfasserin |4 aut | |
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