Steroidal dimer by001 inhibits proliferation and migration of esophageal cancer cells via multiple mechanisms

Wang, Saiqi; Zhou, Kairui; Shi, Xiaoli; Lv, Haiyan; Bie, Liangyu; Zhao, Weijie; Chen, Xiaobing

doi:10.1007/s00280-018-3715-4

Cited by 3 publications

(3 citation statements)

References 23 publications

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“…The cell viability assay was performed on days 1, 2, 3, 4, and 5. The percent of cytotoxicity was calculated using the following formula: %Cell viability = (absorbance of experimental well-absorbance of blank)/(absorbance of untreated control well-absorbance of blank)×100% (12).…”

Section: Cell Viability Detectionmentioning

confidence: 99%

Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer

et al. 2021

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Kremen2 (Krm2) plays an important role in embryonic development, bone formation, and tumorigenesis as a crucial regulator of classical Wnt/β-catenin signaling pathway. However, the role of Krm2 in gastric cancer is not clear. The aim of this study was to explore the regulatory role of Krm2 in the tumorigenesis and metastasis of gastric cancer. It was demonstrated that, compared to para-cancerous tissues, Krm2 was significantly up-regulated in gastric cancer tissues and was positively correlated with the pathological grade of gastric cancer patients. Given that Krm2 is abundantly expressed in most tested gastric cancer cell lines, Krm2 knockdown cell models were established and further used to construct mice xenograft model. After knocking down Krm2, both the cell survival in vitro and tumorigenesis in vivo of gastric cancer cells were inhibited. At the same time, knockdown of Krm2 induced apoptosis, cell cycle arrest at G2/M phase and repression of migration in gastric cancer cells in vitro. Mechanistically, we found that knockdown of Krm2 suppressed PI3K/Akt pathway. Therefore, we revealed the novel role and the molecular mechanism of Krm2 in promoting the tumorigenesis and metastasis in gastric cancer. Krm2 can be a potent candidate for designing of targeted therapy.

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Section: Cell Viability Detectionmentioning

confidence: 99%

Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer

et al. 2021

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“…The JC-1 (Meilun Biotechnology), a fluorescent dye, was used to measure the change of mitochondrial membrane potential (Δ ψ m) 48 . SW620/Ad300 cells were treated with WS-716 (20 μmol/L, 4 h), PTX (1 μmol/L, 2 h), or the combination (preincubated with WS-716 for 2 h before being treated PTX plus WS-716 for 2 h).…”

Section: Methodsmentioning

confidence: 99%

Preclinical studies of the triazolo[1,5-a]pyrimidine derivative WS-716 as a highly potent, specific and orally active P-glycoprotein (P-gp) inhibitor

Wang

Teng

Wang

et al. 2022

Acta Pharmaceutica Sinica B

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“…For instance, Zhen et al 6 revealed that flubendazole impairs the permeability and function of the mitochondrial outer membrane in breast cancer and promotes excessive mitophagy by increasing the DRP1 expression, thereby inhibiting the proliferation and migration of breast cancer cells. In addition, the steroidal dimer by001 inhibits the migration of esophageal cancer by inducing mitophagy 7 . These investigations have shown how autophagy plays dynamic roles in either tumor-suppressive or tumor-promoting ways based on the circumstances and stages of cancer development.…”

Section: Introductionmentioning

confidence: 99%

CREB1 regulates RECQL4 to inhibit mitophagy and promote esophageal cancer metastasis

Zheng,

Zhang,

Gong

et al. 2024

J. Clin. Biochem. Nutr.

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Background: Mitophagy is a cellular survival mechanism that is indispensable in carcinogenesis and tumor progression. However, the research on the mechanism of mitophagy in esophageal cancer metastasis is limited. This study explored the regulatory mechanism by which RECQL4 regulates mitophagy and affects esophageal cancer metastasis. Methods:The RECQL4 expression in esophageal cancer tissues was examined by bioinformatics analysis and validated by qRT-PCR. Bioinformatics analysis was used to determine the upstream regulatory factor of RECQL4, CREB1, and find the correlation between them. Their binding relationship was evaluated using dual luciferase assay and Chromatin Immunoprecipitation (ChIP) assay. The role of

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Steroidal dimer by001 inhibits proliferation and migration of esophageal cancer cells via multiple mechanisms

Cited by 3 publications

References 23 publications

Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer

Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer

Preclinical studies of the triazolo[1,5-a]pyrimidine derivative WS-716 as a highly potent, specific and orally active P-glycoprotein (P-gp) inhibitor

CREB1 regulates RECQL4 to inhibit mitophagy and promote esophageal cancer metastasis

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