Influence of cyclin <scp>D1</scp> splicing variants expression on breast cancer chemoresistance via <scp>CDK4</scp>/<scp>CyclinD1‐pRB‐E2F1</scp> pathway

Wang, Jing; Zhang, Jiaxin; Ma, Qinglong; Zhang, Shasha; Ma, Fengdie; Su, Wei; Zhang, Taotao; Xie, Xiaodong; Chen, Di

doi:10.1111/jcmm.17716

Cited by 7 publications

(5 citation statements)

References 65 publications

(151 reference statements)

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“…CCND1 is a mediator of cell cycle control, and the knockdown of CCND1 splicing variants inhibits cell proliferation and prevents cell cycle progression, thus suppressing chemotherapy resistance in BC cells. 28 In BC cells, IGF1 expression is significantly increased after estrogen treatment, and IGF1 receptor inhibitors inhibit the growth of hormone-resistant BC cells. 29 In BC, SFN protects normal cells from cisplatin-induced toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, we identified CCND1, IGF1, SFN, INHBA, TNNT1, and TNFSF11 as hub genes associated with PTX resistance in BC. CCND1 is a mediator of cell cycle control, and the knockdown of CCND1 splicing variants inhibits cell proliferation and prevents cell cycle progression, thus suppressing chemotherapy resistance in BC cells 28 . In BC cells, IGF1 expression is significantly increased after estrogen treatment, and IGF1 receptor inhibitors inhibit the growth of hormone‐resistant BC cells 29 .…”

Section: Discussionmentioning

confidence: 99%

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Troponin T1 silencing inhibits paclitaxel resistance and the development of breast cancer via suppressing rat sarcoma virus/rapidly accelerated fibrosarcoma 1 pathway

Zhu,

Zhou,

Yang

et al. 2023

Environmental Toxicology

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ObjectiveWe aimed to determine the role of Troponin T1 (TNNT1) in paclitaxel (PTX) resistance and tumor progression in breast cancer (BC).MethodsDifferentially expressed genes were obtained from the GSE4298 and GSE90564 datasets. Hub genes were isolated from protein–protein interaction networks and further validated by real‐time quantitative polymerase chain reaction. The effect of TNNT1 on PTX resistance was determined using cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine, wound healing, transwell, flow cytometry assays, and subcutaneous xenografted tumor model. Western blotting was used to detect proteins associated with PTX resistance, apoptosis, migration, invasion, and other key pathways. Hematoxylin–eosin and immunohistochemical staining were used to evaluate the role of TNNT1 in tumors.ResultsAfter comprehensive bioinformatic analysis, we identified CCND1, IGF1, SFN, INHBA, TNNT1, and TNFSF11 as hub genes for PTX resistance in BC. TNNT1 plays a key role in BC and is upregulated in PTX‐resistant BC cells. TNNT1 silencing inhibited PTX resistance, proliferation, migration, and invasion while promoting apoptosis of PTX‐resistant BC cells. Tumor xenograft experiments revealed that TNNT1 silencing suppresses PTX resistance and tumor development in vivo. In addition, TNNT1 silencing inhibited the expression of proteins in the rat sarcoma virus (RAS)/rapidly accelerated fibrosarcoma1 (RAF1) pathway in vivo. Treatment with a RAS/RAF1 pathway activator reversed the inhibitory effect of TNNT1 silencing on proliferation, migration, and invasion while promoting apoptosis of PTX resistance BC cells.ConclusionSilencing of TNNT1 suppresses PTX resistance and BC progression by inhibiting the RAS/RAF1 pathway, which is a promising biomarker and therapeutic target for drug resistance in BC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Troponin T1 silencing inhibits paclitaxel resistance and the development of breast cancer via suppressing rat sarcoma virus/rapidly accelerated fibrosarcoma 1 pathway

Zhu,

Zhou,

Yang

et al. 2023

Environmental Toxicology

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“…Meanwhile, xenograft tumor assay also confirmed that CDC42EP4 inhibited PCa cell growth in vivo. In addition, it has been reported that E-Cadherin and N-Cadherin, the marker of EMT, are closely associated with tumor invasion [ 29 , 30 ], and CyclinD1 with tumor proliferation [ 31 ]. Our data showed that PCa cells overexpressing CDC42EP4 exhibited high levels of E-cadherin and low levels of N-Cadherin and CyclinD1, suggesting that CDC42EP4 may impair the proliferative and invasive properties of PCa cells.…”

Section: Discussionmentioning

confidence: 99%

Cell division cycle 42 effector protein 4 inhibits prostate cancer progression by suppressing ERK signaling pathway

Zhang,

Yu,

Gao

et al. 2023

Biomol Biomed

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Prostate cancer (PCa) is the most common malignancy among men worldwide. The cell division cycle 42 effector protein 4 (CDC42EP4) functions downstream of CDC42, yet its role and molecular mechanisms in PCa remain unexplored. This study aimed to elucidate the role of CDC42EP4 in the progression of PCa and its underlying mechanisms. Bioinformatical analysis indicated that CDC42EP4 expression was significantly lower in PCa tissue compared to normal prostate tissue. Cellular phenotyping analysis suggested that CDC42EP4 markedly inhibited the proliferation, migration, and invasion of PCa cells. Xenograft tumor assays further demonstrated that CDC42EP4 suppressed the growth of PCa cells in vivo. Mechanistically, the study established that CDC42EP4 inhibited the ERK pathway in PCa cells. Additionally, the ERK pathway inhibitor PD0325901 was employed, revealing that PD0325901 significantly nullified the effects of CDC42EP4 on PCa cell proliferation, migration, and invasion. Collectively, our findings demonstrate that CDC42EP4 acts as a critical tumor suppressor gene, inhibiting PCa cell proliferation, migration, and invasion through the ERK pathway, thereby presenting potential targets for PCa therapy.

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“…This results in the unrestricted entry of free E2F into the cell nucleus, where it interacts with speci c sequences found in gene promoter regions, thereby stimulating the transcription of these genes and giving rise to abnormal cell growth and malignancy. The presence and progression of different types of tumors relies on the signi cant contribution of cyclin D1 [11][12][13][14][15]. Revised sentence: Consequently, the involvement of cyclin D1 is crucial in the onset and advancement of diverse cancer types [11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

“…The presence and progression of different types of tumors relies on the signi cant contribution of cyclin D1 [11][12][13][14][15]. Revised sentence: Consequently, the involvement of cyclin D1 is crucial in the onset and advancement of diverse cancer types [11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Notch signaling pathway promotes invasion of ameloblastoma by regulating E-cadherin via cyclinD1

Gabiyatu,

Li,

Amuersana

et al. 2023

Preprint

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This study aims to investigate the impact of the Notch signaling pathway on the invasion of Ameloblastoma (AM) and its influence on the expression of cyclinD1 protein. AM cells and dental follicle (DF) cells were cultured in vitro. The proliferation activity of two cells were measured using the CCK8. The invasive ability of cells were assessed using the Transwell chamber. A comparison was made between the proliferation and invasion abilities of two cells. The protein expression of cyclinD1, E-cadherin, and Snail was detected using Western Blot. The Notch signaling pathway was blocked using the Notch inhibitor FLI-06.The comparison of proliferation and invasion abilities between two cells were higher than control group cells.The difference was statistically significant (P＜0.05). The Notch inhibitor on the invasive ability of AM cells is significantly lower than control group. The difference was statistically significant (P＜0.05). After intervention with FLI-06, the protein expression of CDK 1, cyclinD1, and Snail in AM cells showed a significant downregulation, while the protein expression of E-cadherin showed a significant upregulation.The Notch signaling pathway plays a crucial role Notch signaling pathway promotes invasion ofAM by regulating E-cadherin via cyclinD1.

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Influence of cyclin D1 splicing variants expression on breast cancer chemoresistance via CDK4/CyclinD1‐pRB‐E2F1 pathway

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 7 publications

References 65 publications

Troponin T1 silencing inhibits paclitaxel resistance and the development of breast cancer via suppressing rat sarcoma virus/rapidly accelerated fibrosarcoma 1 pathway

Troponin T1 silencing inhibits paclitaxel resistance and the development of breast cancer via suppressing rat sarcoma virus/rapidly accelerated fibrosarcoma 1 pathway

Cell division cycle 42 effector protein 4 inhibits prostate cancer progression by suppressing ERK signaling pathway

Notch signaling pathway promotes invasion of ameloblastoma by regulating E-cadherin via cyclinD1

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