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Dihydrotanshinone exerts antitumor effects and improves the effects of cisplatin in anaplastic thyroid cancer cells

ABSTRACT: Dihydrotanshinone exerts antitumor effects and improves the effects of cisplatin in anaplastic thyroid cancer cells

PROVIDER: PRJNA713019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13924092.fastq.gz	Fastqsanger.gz
	SRR13924093.fastq.gz	Fastqsanger.gz
	SRR13924094.fastq.gz	Fastqsanger.gz
	SRR13924095.fastq.gz	Fastqsanger.gz

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Dihydrotanshinone exerts antitumor effects and improves the effects of cisplatin in anaplastic thyroid cancer cells

Project description:Anaplastic thyroid cancer (ATC) is the most aggressive type of thyroid cancer and is responsible for 20-50% of thyroid-associated cancers deaths. The absence of response to conventional treatments makes the search for novel therapeutics an urgent clinical challenge. In the present study, the effects of 15,16-dihydrotanshinone I (DHT), a tanshinone extracted from Salvia miltiorrhiza Bunge (Danshen), which has been shown to possess anticancer activity, were examined on two human ATC cell lines. DHT significantly reduced cell viability, coupled with an increase in apoptosis. DHT administration was also able to reduce the colony-forming ability and the growth in soft agar and downregulate the expression of certain epithelial-to-mesenchymal transition-related genes. In addition, DHT significantly reduced MAD2 expression, a target of HuR with a relevant role in ATC. Finally, cotreatment with cisplatin and DHT augmented their effects on cell viability compared with each compound alone. In conclusion, to the best of our knowledge, the present study is the first to demonstrate that DHT exerts antitumor effects on ATC cells by reducing MAD2 expression levels. Moreover, a synergistic effect of DHT with cisplatin was shown, and thus further in vivo studies are required to assess this phytochemical compound as a potential adjuvant for the treatment of ATC.

2021-03-11 | GSE168616 | GEO

Effects of Dihydrotanshinone I on proliferation and invasiveness of Paclitaxel-resistant anaplastic thyroid cancer cells

Project description:Effects of Dihydrotanshinone I on proliferation and invasiveness of Paclitaxel-resistant anaplastic thyroid cancer cells

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dBET57 exerts anti-cancer effects in neuroblastoma

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Effects of Dihydrotanshinone I on proliferation and invasiveness of Paclitaxel-resistant anaplastic thyroid cancer cells

Project description:ATC is a very rare, but extremely aggressive form of thyroid malignancy, responsible for the highest mortality rate registered for thyroid cancer. In the patients without known genetic aberrations, the current treatment is still represented by palliative surgery and systemic mono- or combined-chemotherapy, which is often not fully effective for appearance of drug resistance. Comprehension of the mechanisms involved in the development of the resistance is therefore an urgent issue to suggest novel therapeutic approaches of this very aggressive malignancy. In this study, we created a model of anaplastic thyroid cancer (ATC) cells resistant to paclitaxel, to investigate the characteristics of these cells by analyzing the profile of gene expression and comparing with that of paclitaxel-sensitive original ATC cell lines. In addition, we evaluated the effects of Dihydrotanshinone I (DHT) on the viability and invasiveness of paclitaxel-resistant cells. ATC paclitaxel-resistant cells highlighted an overexpression of ABCB1 and a hyper-activation of the NF-κB compared to sensitive cells. DHT treatment results in a reduction of cell viability, and clonogenic ability of resistant cells. Moreover, DHT induces a decrement of NF-κB activity in SW1736-PTX and 8505C-PTX cells. In conclusion, to the best of our knowledge, the results of the present study are the first to demonstrate the antitumor effects of DHT on ATC cells resistant to Paclitaxel in vitro.

2021-07-10 | GSE179786 | GEO

Effects of BRAF and ERK inhibition on papillary and anaplastic thyroid cancer

Project description:To investigate the effects of combined BRAF inhibition (dabrafenib) and ERK inhibition (ulixertinib) on papillary and anaplastic thyroid cancer transcriptional reprogramming

2023-06-15 | GSE221329 | GEO

Curcumin exerts its potential antitumor effects in a context dependent fashion

Project description:Background Clinical practice demonstrates that anticancer drug effects may strongly vary between different patients. Individual responses to drug action are potentially responsible for adverse effects such as establishment of resistance. Consequently, the understanding of response mechanisms to drug actions is of great relevance. Proteome profiling is a powerful tool for the investigation of cellular responses to drugs. Methods Here, we have investigated the effects of curcumin, a natural remedy with known anti-cancer activities, on breast cancer cells MCF-7, ZR-75-1 and normal mammary fibroblasts as well as co-cultures thereof using proteome profiling. The mammary fibroblasts had been treated before with TGF-beta in order to induce a wound-healing signature known to be representative for the in vivo situation in breast tumors. Results While co-culture alone induced several proteins like ANXA1, S100A4 and SPARC similarly in both breast cancer cells, the majority of proteins regulated upon co-culture differed between MCF-7 and ZR-75-1. Curcumin significantly induced HMOX1 in all single cell models and co-cultures. However, otherwise the curcumin effects differed. In the MCF-7 co-culture, curcumin significantly downregulated RC3H1, a repressor of inflammatory signaling. In the ZR-75-1 co-culture, curcumin significantly downregulated PEG10, an anti-apoptotic protein, and induced RRAGA, a pro-apoptotic protein involved in TNF-alpha signaling. In this model, curcumin also induced AKR1C2, an important enzyme for progesterone metabolism. None of these specific curcumin effects were observed in single cell cultures. Conclusions The present data demonstrate that curcumin induces proteome alterations potentially accounting for its known antitumor effects in a strongly context-dependent fashion.

2018-06-04 | PXD008719 | Pride

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BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

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