Dual cyclin‐dependent kinase 4/6 inhibition by PD‐0332991 induces apoptosis and senescence in oesophageal squamous cell carcinoma cells

Chen, Liang; Pan, Jingxuan

doi:10.1111/bph.13836

Cited by 45 publications

(51 citation statements)

References 60 publications

(74 reference statements)

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“…C-D, Pristimerin blocked the nuclear translocation of p65 stimulated by TNFα in ESCC cells. 27 2.6 | Cell viability assay EC9706, EC109, and KYSE30 were treated with escalating concentrations of pristimerin for 72 hours; cell viability was determined by MTS assay, and 50% inhibition of cell growth (IC 50 ) was evaluated. DAPI was used to stain the nuclear.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…27 The migrated or invaded cells were fixed with 3% paraformaldehyde for 20 minutes and then stained by crystal violet for 10 minutes. The cells were then cultured in the top chamber of transwell covered with (invasion) or without (migration) matrigel in the absence of FBS, while DMEM was added in the bottom well containing 20% FBS as chemoattract factor.…”

Section: Migration and Invasion Assaymentioning

confidence: 99%

“…25 All the protein samples were then analysed by western blotting as described previously. 27 2.6 | Cell viability assay EC9706, EC109, and KYSE30 were treated with escalating concentrations of pristimerin for 72 hours; cell viability was determined by MTS assay, and 50% inhibition of cell growth (IC 50 ) was evaluated.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…The cells were then cultured in the top chamber of transwell covered with (invasion) or without (migration) matrigel in the absence of FBS, while DMEM was added in the bottom well containing 20% FBS as chemoattract factor. 27 The migrated or invaded cells were fixed with 3% paraformaldehyde for 20 minutes and then stained by crystal violet for 10 minutes. The cells in 3 randomly were photographed and counted.…”

Section: Migration and Invasion Assaymentioning

confidence: 99%

“…PBS) were subcutaneously implanted on the flanks of each mouse as described before 27. Tumours were measured every other day and calculated with the following formula:a 2 × b × 0.4,where a is the smallest diameter and b is the diameter perpendicular to a.…”

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confidence: 99%

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Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

Tan

Zhou

et al. 2018

Cell Biochemistry & Function

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Although several approaches including surgery, chemotherapy, and radiotherapy had been applied in the treatment of ESCC, more effective targeted chemotherapies are required to increase the survival rates of patients. This study suggested that inhibiting NF-κB signalling pathway could be an effective approach for the treatment of ESCC. Pristimerin, a potent NF-κB inhibitor, exerted potent anti-ESCC effects both in vitro and in vivo, which may be a promising therapeutic agent for ESCC.

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Section: Western Blot Analysismentioning

confidence: 99%

Section: Migration and Invasion Assaymentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Migration and Invasion Assaymentioning

confidence: 99%

mentioning

confidence: 99%

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Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

Tan

Zhou

et al. 2018

Cell Biochemistry & Function

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NEK2 Promotes ESCC Malignant Progression by Inhibiting Cellular Senescence via the FOXM1/c‐Myc/p27 Signaling Pathway

Li,

Wang,

Wei

et al. 2024

Molecular Carcinogenesis

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Never in mitosis gene A (NIMA)‐related kinase 2 (NEK2) is a crucial serine‐threonine kinase involved in the process of cell mitosis. However, the precise relationship between NEK2 and esophageal squamous cell carcinoma (ESCC) remains inadequately understood. NEK2 expression in ESCC tissues was assessed through bioinformatics analysis, reverse transcription‐quantitative PCR (RT‐qPCR) and immunohistochemistry, revealing a correlation with ESCC patient prognosis. Cultured ESCC cells and human normal esophageal epithelial cells (HEEC) were used to investigate the effects of NEK2 knockdown on the development and progression of ESCC by integrated confluence algorithm, colony formation, wound‐healing, transwell, and ESCC xenograft tumor model, in vitro and in vivo. In ESCC tissues, NEK2 was found to be significantly upregulated, and its expression correlated with poor prognosis in ESCC patients. NEK2 may facilitate ESCC development by regulating cell proliferation, migration, and invasion. Additionally, results from in vivo experiments suggested that NEK2 knockdown can inhibit tumor growth. Moreover, forkhead box M1 (FOXM1) was identified as a potential downstream target of NEK2 in the regulation of ESCC, with its overexpression reversing the effects of NEK2 knockdown on ESCC. Mechanistic studies also indicated that NEK2 may promote the malignant progression of ESCC by inhibiting cellular senescence through the activation of the FOXM1/c‐Myc/p27 signaling pathways, which may provide a novel perspective for the management of ESCC.

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Molecular mechanisms of chemo‐ and radiotherapy resistance and the potential implications for cancer treatment

Liu

Zheng

Huang

et al. 2021

MedComm

189

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Cancer is a leading cause of death worldwide. Surgery is the primary treatment approach for cancer, but the survival rate is very low due to the rapid progression of the disease and presence of local and distant metastasis at diagnosis. Adjuvant chemotherapy and radiotherapy are important components of the multidisciplinary approaches for cancer treatment. However, resistance to radiotherapy and chemotherapy may result in treatment failure or even cancer recurrence. Radioresistance in cancer is often caused by the repair response to radiation‐induced DNA damage, cell cycle dysregulation, cancer stem cells (CSCs) resilience, and epithelial‐mesenchymal transition (EMT). Understanding the molecular alterations that lead to radioresistance may provide new diagnostic markers and therapeutic targets to improve radiotherapy efficacy. Patients who develop resistance to chemotherapy drugs cannot benefit from the cytotoxicity induced by the prescribed drug and will likely have a poor outcome with these treatments. Chemotherapy often shows a low response rate due to various drug resistance mechanisms. This review focuses on the molecular mechanisms of radioresistance and chemoresistance in cancer and discusses recent developments in therapeutic strategies targeting chemoradiotherapy resistance to improve treatment outcomes.

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Dual cyclin‐dependent kinase 4/6 inhibition by PD‐0332991 induces apoptosis and senescence in oesophageal squamous cell carcinoma cells

Cited by 45 publications

References 60 publications

Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

Pristimerin targeting NF‐κB pathway inhibits proliferation, migration, and invasion in esophageal squamous cell carcinoma cells

NEK2 Promotes ESCC Malignant Progression by Inhibiting Cellular Senescence via the FOXM1/c‐Myc/p27 Signaling Pathway

Molecular mechanisms of chemo‐ and radiotherapy resistance and the potential implications for cancer treatment

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