Hydroxychloroquine enhances the antitumor effects of BC001 in gastric cancer

Wang, Wei; Liu, Linqing; Zhou, Yucheng; Ye, Qiang; Yang, Xiuli; Jiang, Jialiang; Ye, Ziqi; Gao, Feng; Tan, Xiaolu; Zhang, Guobing; Fang, Qingxia; Xuan, Zixue

doi:10.3892/ijo.2019.4824

Cited by 19 publications

(12 citation statements)

References 28 publications

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“…After treated with curcumin (1 μM and 5 μM) or rapamycin (100 nM) for 24 h, the LGR5(+) colorectal CSCs were washed twice with ice-cold PBS, fixed using 2.5% glutaraldehyde for 60 min at room temperature, and post-fixed in 1% osmium tetroxide for 30 min. As described previously [ 19 , 20 ], all samples were embedded in EPON resin and stained with uranyl acetate and lead citrate. The cells were observed under a transmission electron microscope (H-7650; Hitachi High-Technologies Corp., Tokyo, Japan).…”

Section: Colorectal Cscsmentioning

confidence: 99%

Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway

et al. 2021

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Colorectal cancer stem cells (CSCs) have the potential for self-renewal, proliferation, and differentiation. And LGR5 is a stem cell marker gene of colorectal cancer. Curcumin can suppress oncogenicity of many cancer cells, yet the effect and mechanism of curcumin in LGR5(+) colorectal cancer stem cells (CSCs) have not been studied. In this study, we studied the effect of curcumin on LGR5(+) colorectal CSCs using the experiments of tumorsphere formation, cell viability and cell apoptosis. Then autophagy analysis, RNA-Seq, and real-time PCR were used to identify the mechanism responsible for the inhibition of LGR5(+) colorectal CSCs. Our results showed that curcumin inhibited tumorsphere formation, decreased cell viability in a dose-dependent manner, and also promoted apoptosis of LGR5(+) colorectal CSCs. Next, we found curcumin induced autophagy of LGR5(+) colorectal CSCs. When LGR5(+) colorectal CSCs were co-treated with curcumin and the autophagy inhibitor (hydroxychloroquine), curcumin-induced cell proliferation inhibition decreased. In addition, we also found that curcumin inhibited the extracellular matrix (ECM)-receptor interaction pathway via the downregulation of the following genes: GP1BB, COL9A3, COMP, AGRN, ITGB4, LAMA5, COL2A1, ITGB6, ITGA1, and TNC. Further, these genes were transcriptionally regulated by TFAP2A, and the high expression of TFAP2A was associated with poor prognosis in colorectal cancer. In conclusion, curcumin suppressed LGR5(+) colorectal CSCs, potentially by inducing autophagy and repressing the oncogenic TFAP2A-mediated ECM pathway. Graphic abstract

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Section: Colorectal Cscsmentioning

confidence: 99%

Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway

et al. 2021

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“…Western blot analysis was performed as previously described ( 24 ). The primary antibodies used in the present study were anti-FTO (1,1000; ab124892; Abcam) and anti-β-actin (1:200; ab115777; Abcam).…”

Section: Methodsmentioning

confidence: 99%

Fat mass and obesity-associated protein promotes the tumorigenesis and development of liver cancer

Wang²,

Chen

et al. 2020

Oncol Lett

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Liver cancer is the fourth leading cause of cancer-associated mortality worldwide. Statistics indicate that the incidence of liver cancer has been increasing and that its prognosis remains poor. Fat mass and obesity-associated protein (FTO) is a demethylase that is involved in N6-methyladenosine (m6a) RNA modification; however, to the best of our knowledge, its role in tumorigenesis and development of liver cancer remains unknown. In the present study, cell proliferation, colony formation, apoptosis, Transwell and wound healing assays of small interfering (si)RNA-FTO HepG2 cells were performed, and the levels of m6A RNA methylation were assessed. Additionally, the prognostic value of FTO in liver cancer was analyzed using immunohistochemistry analysis. The results from the EpiQuik m6A RNA methylation quantitative assay revealed that knockdown of FTO increased the total m6A methylation level. Notably, FTO promoted the proliferation and migration of liver cancer cells. Additionally, FTO expression was upregulated in patients with liver cancer and was associated with a high Edmondson Grade, which served as an independent prognostic factor for liver cancer. Results from the Kaplan-Meier survival analysis revealed that low expression levels of FTO predicted a good prognosis. The 5-year overall survival of the low FTO expression group was 68% compared with 48% in the high FTO expression group (P=0.077). In conclusion, the present study suggested that FTO regulates the tumorigenesis and development of liver cancer.

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“…It was found that inhibition of hypoxic signaling, via VEGFR2, in combination with hydroxychloroquine can enhance the therapeutic effect and thus killing of gastric cancer cells [201]. Salidroside, a natural ingredient derived from the Rhodiola rosea species, decreased the phosphorylation of PI3K and thus induced autophagy [202]. Induction of autophagy caused a protective effect towards the gastric cells and the addition of hydroxychloroquine caused cell induced apoptosis [201].…”

Section: Mtor-dependent Signaling Pathwaysmentioning

confidence: 99%

Gastric cancer: a comprehensive review of current and future treatment strategies

Sexton

Hallak

Diab

et al. 2020

Cancer Metastasis Rev

357

251

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Gastric cancer remains a major unmet clinical problem with over 1 million new cases worldwide. It is the fourth most commonly occurring cancer in men and the seventh most commonly occurring cancer in women. A major fraction of gastric cancer has been linked to variety of pathogenic infections including but not limited to Helicobacter pylori (H. pylori) or Epstein Barr virus (EBV). Strategies are being pursued to prevent gastric cancer development such as H. pylori eradication, which has helped to prevent significant proportion of gastric cancer. Today, treatments have helped to manage this disease and the 5-year survival for stage IA and IB tumors treated with surgery are between 60 and 80%. However, patients with stage III tumors undergoing surgery have a dismal 5-year survival rate between 18 and 50% depending on the dataset. These figures indicate the need for more effective molecularly driven treatment strategies. This review discusses the molecular profile of gastric tumors, the success, and challenges with available therapeutic targets along with newer biomarkers and emerging targets.

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Hydroxychloroquine enhances the antitumor effects of BC001 in gastric cancer

Cited by 19 publications

References 28 publications

Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway

Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway

Fat mass and obesity-associated protein promotes the tumorigenesis and development of liver cancer

Gastric cancer: a comprehensive review of current and future treatment strategies

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