Knockdown of PVT1 inhibits cell proliferation in luminal and basal-like breast cancer subtypes by activating LATS2/Hippo signaling pathway DOI
Haibo Zhang, Ying Zeng, Guo Wang

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 9, 2025

Abstract Background: Breast cancer (BC) is a malignant tumor seriously threatening women’s health, while current approaches to BC treatment are challenged by the existence of drug resistance. Combination strategies targeted therapy have been successfully applied in clinical treatment. However, whether there exist critical long non-coding RNAs (lncRNAs) responsible for pathogenesis and representing promising candidates combined remains an issue. Methods: Public databases bioinformatic methods were used identify lncRNAs abnormally expressed among different subtypes BC. The expression level PVT1 was verified collected samples representative cell lines. role proliferation examined using MTS, plate clone formation, EdU flow cytometry assay after small interfering RNA (siRNA) sequencing performed investigate potential molecular events regulated PVT1. Western blot immunofluorescence experiments verify activation LATS2/Hippo signaling pathway knockdown. In addition, its confirmed mediate function through rescue assay. regulatory effect on LATS2 investigated mRNA stability experiments. Results: The tissues luminal basal-like significantly higher than that paracancerous tissues. knockdown substantially inhibited cells both subtypes. revealed Hippo might be downstream target After knockdown, protein elevated which further decreased distribution YAP nucleus, indicating pathway. inhibitory could attenuated simultaneous LATS2. Furthermore, demonstrated slow down degradation rate mRNA. Conclusions: PVT1 Knockdown inhibit these two partly activating

Language: Английский

Knockdown of PVT1 inhibits cell proliferation in luminal and basal-like breast cancer subtypes by activating LATS2/Hippo signaling pathway DOI
Haibo Zhang, Ying Zeng, Guo Wang

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 9, 2025

Abstract Background: Breast cancer (BC) is a malignant tumor seriously threatening women’s health, while current approaches to BC treatment are challenged by the existence of drug resistance. Combination strategies targeted therapy have been successfully applied in clinical treatment. However, whether there exist critical long non-coding RNAs (lncRNAs) responsible for pathogenesis and representing promising candidates combined remains an issue. Methods: Public databases bioinformatic methods were used identify lncRNAs abnormally expressed among different subtypes BC. The expression level PVT1 was verified collected samples representative cell lines. role proliferation examined using MTS, plate clone formation, EdU flow cytometry assay after small interfering RNA (siRNA) sequencing performed investigate potential molecular events regulated PVT1. Western blot immunofluorescence experiments verify activation LATS2/Hippo signaling pathway knockdown. In addition, its confirmed mediate function through rescue assay. regulatory effect on LATS2 investigated mRNA stability experiments. Results: The tissues luminal basal-like significantly higher than that paracancerous tissues. knockdown substantially inhibited cells both subtypes. revealed Hippo might be downstream target After knockdown, protein elevated which further decreased distribution YAP nucleus, indicating pathway. inhibitory could attenuated simultaneous LATS2. Furthermore, demonstrated slow down degradation rate mRNA. Conclusions: PVT1 Knockdown inhibit these two partly activating

Language: Английский

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