cholangiocarcinoma cell
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Author(s):  
Jisen Zhao ◽  
Yang Yu ◽  
Wang Yan ◽  
Shujie Cheng

IntroductionOne of the simplest nanostructures that is widely used in industry today is metallic nanoparticles. Metallic ‎nanoparticles can bind non-destructively to single-stranded DNA, which are important in medical diagnostics. ‎Cancer nanotechnology developed a new area of integrative research in biology, chemistry, engineering, and ‎medicine, and is concerned with major advances in cancer diagnosis, prevention and treatment ‎Material and methods‎ In the recent study, the structural and morphological characterization of bio‐synthesized FeNPs@Calendula ‎arvensis was performed by FT-IR and UV-vis spectroscopy, scanning electron microscopy (SEM) that SEM ‎images have exhibited an equal and uniform spherical morphology in size of 30.13 nm. ‎ResultsIn the antioxidant test, the IC50 of FeNPs@Calendula arvensis and BHT against DPPH free radicals were 117 ‎and 88 µg/mL, respectively. In the anticancer test, the treated cells with FeNPs@Calendula arvensis were ‎assessed by MTT assay for 48h about the anti-human cholangiocarcinoma and ‎ cytotoxicity properties on normal ‎‎(HUVEC) and cholangiocarcinoma ‎ carcinoma cell lines i.e., HCM-CSHL-0174-C22, CCLP-1, and QBC939. ‎The IC50 of FeNPs@Calendula arvensis were 196, 237, and 278 µg/mL against HCM-CSHL-0174-C22, ‎CCLP-1, and QBC939‎ cell lines, respectively. The viability of cholangiocarcinoma cell line reduced dose-‎dependently in the presence of FeNPs@Calendula arvensis.‎ConclusionsIt appears that the anti-human cholangiocarcinoma effect of FeNPs@Calendula arvensis is due to their ‎antioxidant effects.‎


Author(s):  
Yang Yang ◽  
Jigang Li ◽  
Lei Yao ◽  
Lile Wu

Cholangiocarcinoma is a relatively rare neoplasm with increasing incidence. Although chemotherapeutic agent such as gemcitabine has long been used as standard treatment for cholangiocarcinoma, the interindividual variability in target and drug sensitivity and specificity may lead to therapeutic resistance. In the present study, we found that photodynamic therapy (PDT) treatment inhibited gemcitabine-resistant cholangiocarcinoma cells via repressing cell viability, enhancing cell apoptosis, and eliciting G1 cell cycle arrest through modulating Cyclin D1 and caspase 3 cleavage. In vivo, PDT treatment significantly inhibited the growth of gemcitabine-resistant cholangiocarcinoma cell-derived tumors. Online data mining and experimental analyses indicate that KLF10 expression was induced, whereas EGFR expression was downregulated by PDT treatment; KLF10 targeted the EGFR promoter region to inhibit EGFR transcription. Under PDT treatment, EGFR overexpression and KLF10 silencing attenuated the anti-cancer effects of PDT on gemcitabine-resistant cholangiocarcinoma cells by promoting cell viability, inhibiting apoptosis, and increasing S phase cell proportion. Importantly, under PDT treatment, the effects of KLF10 silencing were significantly reversed by EGFR silencing. In conclusion, PDT treatment induces KLF10 expression and downregulates EGFR expression. KLF10 binds to EGFR promoter region to inhibit EGFR transcription. The KLF10/EGFR axis participates in the process of the inhibition of PDT on gemcitabine-resistant cholangiocarcinoma cells.


2021 ◽  
Vol 22 (11) ◽  
pp. 3633-3640
Author(s):  
Pongsakorn Martviset ◽  
Luxsana Panrit ◽  
Pathanin Chantree ◽  
Phunuch Muhamad ◽  
Kesara Na-Bangchang

Life Sciences ◽  
2021 ◽  
pp. 120072
Author(s):  
Nathakan Klinhom-on ◽  
Wunchana Seubwai ◽  
Kanlayanee Sawanyawisuth ◽  
Sumalee Obchoei ◽  
Panupong Mahalapbutr ◽  
...  

2021 ◽  
Vol 41 (10) ◽  
pp. 4917-4928
Author(s):  
SUPAPORN YANGNGAM ◽  
SUYANEE THONGCHOT ◽  
KULTHIDA VAETEEWOOTTACHARN ◽  
PETI THUWAJIT ◽  
MARCELA A. HERMOSO ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Huayuan Liu ◽  
Caiyun Liu ◽  
Mengya Wang ◽  
Dongxu Sun ◽  
Pengcheng Zhu ◽  
...  

AbstractIn the present study, we aimed to find the target of Tanshinone IIA (Tan-IIA) in Cholangiocarcinoma by network pharmacology-based prediction and investigate the possible mechanism through experimental verification. In this study, we combined Tan-IIA-specific and Cholangiocarcinoma-specific targets with protein–protein interactions (PPI) to construct a Tan-IIA targets-Cholangiocarcinoma network, and network pharmacology approach was applied to identify potential targets and mechanisms of Tan-IIA in the treatment of Cholangiocarcinoma. The anti-cancer effects of Tan-IIA were investigated by using subcutaneous tumorigenic model in nude mice and in the human Cholangiocarcinoma cell lines in vitro. Our results showed that Tan-IIA treatment considerably suppressed the proliferation and migration of Cholangiocarcinoma cells while inducing apoptosis of Cholangiocarcinoma cells. Western blot results demonstrated that the expression of PI3K, p-Akt, p-mTOR, and mTOR were inhibited by Tan-IIA. Meanwhile, After treatment with Tan-IIA, the level of Bcl2 was downregulated and cleaved caspase-3 expression increased. Further studies revealed that the anticancer effects of Tan-IIA were severely mitigated by pretreatment with a PI3K agonist. Our research provides a new anticancer strategy and strengthens support for the use of Tan-IIA as an anticancer drug for the treatment of CCA.


Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4774
Author(s):  
Giulia Anichini ◽  
Laura Carrassa ◽  
Barbara Stecca ◽  
Fabio Marra ◽  
Chiara Raggi

Cholangiocarcinoma (CCA) is a poorly treatable type of cancer and, along with hepatocellular carcinoma (HCC), is the predominant type of primitive liver cancer in adults. The lack of understanding of CCA biology has slowed down the identification of novel targets and the development of effective treatments. While tumors share some general characteristics, detailed knowledge of specific features is essential for the development of effectively tailored therapeutic approaches. The Hedgehog (HH) signaling cascade regulates stemness biology, embryonal development, tissue homeostasis, and cell proliferation and differentiation. Its aberrant activation has been associated with a variety of solid and hematological human malignancies. Several HH-inhibiting compounds have been indeed developed as potential anticancer agents in different types of tumors, with Smoothened and GLI inhibitors showing the most promising results. Beside its well-established function in other tumors, findings regarding the HH signaling in CCA are still controversial. Here we will give an overview of the most important clinical and molecular features of cholangiocarcinoma, and we will discuss the available evidence of the crosstalk between the HH signaling pathway and the cholangiocarcinoma cell biology.


Author(s):  
Nattapong Puthdee ◽  
Sira Sriswasdi ◽  
Trairak Pisitkun ◽  
Sutheera Ratanasirintrawoot ◽  
Nipan Israsena ◽  
...  

AbstractCholangiocarcinoma (CCA), a lethal malignancy of the biliary epithelium, is the second most common primary liver cancer. The poor prognosis of CCA is due to the high rate of tumour invasion and distant metastasis. We found that the RNA-binding protein LIN28B, a known regulator of microRNA biogenesis, stem cell maintenance, and oncogenesis, is expressed in a subpopulation of CCA patients. To further investigate the potential role of LIN28B in CCA pathogenesis, we studied the effect of LIN28B overexpression in the cholangiocyte cell line MMNK-1 and cholangiocarcinoma cell lines HuCCT-1 and KKU-214. Here, we show that enhanced LIN28B expression promoted cancer stem cell-like properties in CCA, including enhanced cell migration, epithelial-to-mesenchymal transition (EMT), increased cell proliferation and spheroid formation. Proteomic analysis revealed TGF-β-induced protein (TGFBI) as a novel LIN28B target gene, and further analysis showed upregulation of other components of the TGF-β signalling pathway, including TGF-β receptor type I (TGFBRI) expression and cytokine TGFB-I, II and III secretion. Importantly, the small molecule TGF-β inhibitor SB431542 negated the effects of LIN28B on both cell migration and clonogenic potential. Overexpression of TGFBI alone promoted cholangiocarcinoma cell migration and EMT changes, but not spheroid formation, suggesting that TGFBI partially contributes to LIN28B-mediated aggressive cell behaviour. These observations are consistent with a model in which TGF-β and LIN28B work together to form a positive feedback loop during cholangiocarcinoma metastasis and provide a therapeutic intervention opportunity.


2021 ◽  
Author(s):  
Yihang Zhao ◽  
Yaxian Kuai ◽  
Jianhua Xu ◽  
Yufang Cui ◽  
Juan Wu ◽  
...  

Abstract BackgroundCholangiocarcinoma (CCA), is a rare biliary adenocarcinoma associated with poor outcomes. Deacetylase Sirtuin‐3 (SIRT3), a histone deacetylase (HDAC), has been considered to be associated with various cancers and can be a potential new target for CCA.We intended to identify the target of SIRT3 and explore the mechanism of SIRT3 in CCA.MethodsThe expression levels of SIRT3 and hypoxia‐inducible factor‐1α (HIF1α) in CCA tissues and cell lines were examined by RT-qPCR. CCK-8 and EdU methods were used to detect cell proliferation in CCA. To assess the levels of proteins related to cell proliferation and epithelial-mesenchymal transition (EMT) process, western blot analysis was conducted. Co-Immunoprecipitation and deacetylation assays were used to explore HIF1α protein acetylation, stability and the relationship between SIRT3 and HIF1α in CCA cells.ResultsSIRT3 showed low expression in CCA tissues and cells. SIRT3 overexpression inhibited cell proliferation and EMT process. Moreover, the interaction between SIRT3 and HIF1α was confirmed and HIF1α expression was negatively regulated by SIRT3. Furthermore, we also found that HIF1α was more easily degraded and showed a reduction in stability through deacetylation via SIRT3 knockdown. In rescue assays, HIF1α also reversed the inhibitory effect of SIRT3 on cell proliferation and the EMT process. ConclusionsSIRT3 suppressed cell proliferation and the EMT process in CCA by targeting HIF1α.Trial registrationSamples were obtained only after the patient has given informed consent according to the established plan approved by the Ethics Committee of The First Affiliated Hospital of Anhui Medical University.


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