Rabdocoestin B exhibits antitumor activity by inducing G2/M phase arrest and apoptosis in esophageal squamous cell carcinoma

Wang, Jingnan; Zhang, Zhirong; Cao, Yun; Yuan, Zuyang; Lu, Zhiliang; Li, Yuan; Wan, Jun; Sun, Han‐Dong; Chen, Zhaoli; Pu, Jian‐Xin; He, Jie

doi:10.1007/s00280-017-3507-2

Cited by 4 publications

(2 citation statements)

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“…UEB2C directly interferes with the level of cyclin B1 protein and alters the proliferation and cell cycle characteristics of ESCC ( 66 ). Due to activation of the p53/p21 pathway, CDC25C is thus reduced, leading to cell cycle arrest ( 67 , 68 ). Although the quantity and quality of PPI data have greatly improved in recent years, the human PPI network is far from being completed.…”

Section: Discussionmentioning

confidence: 99%

Network and pathway-based analysis of genes associated with esophageal squamous cell carcinoma

He¹,

Yuan²,

He³

et al. 2023

Ann Transl Med

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Background Although diagnostic methods and treatments have improved over the last few years, the 5-year survival rate of esophageal squamous cell carcinoma (ESCC) patients remains generally poor. The development of high-throughput technology has facilitated great achievements in localization of ESCC-related genes. To take a further step toward a thorough understanding of ESCC at a molecular level, the potential pathogenesis of ESCC needs to be deciphered. Methods The interaction of ESCC-related genes was explored by collecting genes associated with ESCC and then performing gene enrichment assays, pathway enrichment assays, pathway crosstalk analysis, and extraction of ESCC-specific subnetwork to describe the relevant biochemical processes. Results Through Gene Ontology (GO) enrichment analysis, many molecular functions related to response to chemical, cellular response to stimulus, and cell proliferation were found to be significantly enriched in ESCC-related genes. The results of pathway and pathway crosstalk analysis showed that pathways associated with multiple malignant tumors, the immune system, and metabolic processes were significantly enriched in ESCC-related genes. Through the analysis of specific subnetworks, we obtained some novel ESCC-related potential genes, such as MUC13 , GSTO1 , FIN , GRB2 , CDC25C , and others. Conclusions The molecular mechanism of ESCC is extremely complex. Some inducing factors change the expression status of many genes. The abnormal expression of genes mediates the biological processes involved in immunity and metabolism, apoptosis, and cell proliferation, leading to the occurrence of tumors. The genes MUC13 , RYK , and FIN may be potential prognostic indicators of ESCC; GRB2 and CDC25C may be potential targets of ESCC in proliferation. Our work may provide valuable information for further understanding the molecular mechanisms for the development of ESCC.

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Section: Discussionmentioning

confidence: 99%

Network and pathway-based analysis of genes associated with esophageal squamous cell carcinoma

He¹,

Yuan²,

He³

et al. 2023

Ann Transl Med

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show abstract

“…One of the least studied yet very aggressive cancers is esophageal cancer [ 31 , 32 , 33 , 34 ]. Although it is the 8th most common type of cancer, it is the 6th leading cancer in terms of cancer deaths [ 32 , 33 , 34 ]. Esophageal squamous cell carcinoma (ESCC) is the predominant histological cancer type in Africa, Asia, and Latin America.…”

Section: Introductionmentioning

confidence: 99%

Chemoresistance to Cancer Treatment: Benzo-α-Pyrene as Friend or Foe?

et al. 2018

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Background: Environmental pollution such as exposure to pro-carcinogens including benzo-α-pyrene is becoming a major problem globally. Moreover, the effects of benzo-α-pyrene (BaP) on drug pharmacokinetics, pharmacodynamics, and drug resistance warrant further investigation, especially in cancer outpatient chemotherapy where exposure to environmental pollutants might occur. Method: We report here on the effects of benzo-α-pyrene on esophageal cancer cells in vitro, alone, or in combination with chemotherapeutic drugs cisplatin, 5-flurouracil, or paclitaxel. As the study endpoints, we employed expression of proteins involved in cell proliferation, drug metabolism, apoptosis, cell cycle analysis, colony formation, migration, and signaling cascades in the WHCO1 esophageal cancer cell line after 24 h of treatment. Results: Benzo-α-pyrene had no significant effect on WHCO1 cancer cell proliferation but reversed the effect of chemotherapeutic drugs by reducing drug-induced cell death and apoptosis by 30–40% compared to drug-treated cells. The three drugs significantly reduced WHCO1 cell migration by 40–50% compared to control and BaP-treated cells. Combined exposure to drugs was associated with significantly increased apoptosis and reduced colony formation. Evaluation of survival signaling cascades showed that although the MEK-ERK and Akt pathways were activated in the presence of drugs, BaP was a stronger activator of the MEK-ERK and Akt pathways than the drugs. Conclusion: The present study suggest that BaP can reverse the effects of drugs on cancer cells via the activation of survival signaling pathways and upregulation of anti-apoptotic proteins such as Bcl-2 and Bcl-xL. Our data show that BaP contribute to the development of chemoresistant cancer cells.

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Perspectives and mechanisms for targeting mitotic catastrophe in cancer treatment

Bai,

Zhou,

Peng

et al. 2023

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Rabdocoestin B exhibits antitumor activity by inducing G2/M phase arrest and apoptosis in esophageal squamous cell carcinoma

Abstract: Taken together, these findings indicate that Rabd-B is a promising precursor compound that may be useful as a treatment for ESCC and thus warrants further investigation.

Cited by 4 publications

References 50 publications

Network and pathway-based analysis of genes associated with esophageal squamous cell carcinoma

Network and pathway-based analysis of genes associated with esophageal squamous cell carcinoma

Chemoresistance to Cancer Treatment: Benzo-α-Pyrene as Friend or Foe?

Perspectives and mechanisms for targeting mitotic catastrophe in cancer treatment

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