Emerging Drugs in Refractory Colorectal Cancer

Nobili, Stefania; Galletta, Alessandro; Brugia, Marco; Tassi, Renato; Petreni, Paolo; Landini, Ida; Mini, Enrico

doi:10.4155/fmc.15.85

Cited by 3 publications

(2 citation statements)

References 33 publications

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“…Exosomal miR-19b participates in oxaliplatin sensitivity. Based on the results of Fang et al [22], 10 miRNAs were selected, and QPCR was used to analyze the differences in levels between untreated sw480 cells and sw480 cells treated with 20 μM oxaliplatin for an extended period [21]. miR-19b was the miRNA which attracted our attention ( Figure 3A), because our previous studies proved that miR-19b functions as an oncogene in lung cancer and breast cancer [23], and miR-19a also functions similarly in colorectal cancer [24].…”

Section: Oxaliplatin Inhibits Proliferation Of Sw480 Cellsmentioning

confidence: 99%

Suppressing the secretion of exosomal miR-19b by gw4869 could regulate oxaliplatin sensitivity in colorectal cancer

Gu¹,

Yu²,

Zhang³

et al. 2019

neo

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Oxaliplatin is commonly used in managing malignancy, including colorectal cancer. While treatment often fails due to decreased drug sensitivity, the mechanisms involved are not clear. In this study, we investigate how exosomal miR-19b participates in oxaliplatin sensitivity and then prove that miR-19b down-regulates oxaliplatin sensitivity of sw480 cells. We found that suppressing the secretion of exosomal miR-19b with gw4869 promotes sw480 cell oxaliplatin sensitivity. Our combined results demonstrate for the first time that miR-19b regulates the oxaliplatin sensitivity of sw480 cells and provides a unique mechanism mediated by gw4869 to modulate oxaliplatin sensitivity by suppressing exosomal miR-19b release.

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Section: Oxaliplatin Inhibits Proliferation Of Sw480 Cellsmentioning

confidence: 99%

Suppressing the secretion of exosomal miR-19b by gw4869 could regulate oxaliplatin sensitivity in colorectal cancer

Gu¹,

Yu²,

Zhang³

et al. 2019

neo

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“…Due to the higher incidence and mortality of CRC, investigators have paid more attention on its pathogenic mechanism, as well as the identification of novel anti-CRC drugs 16 , 17 . Previous studies revealed that many natural products can inhibit the development, the identification of more efficient anti-tumor drugs, and also the understanding of underlying molecular mechanisms is also necessary because of the complex pathogenic mechanism in CRC.…”

Section: Discussionmentioning

confidence: 99%

Cincumol prevents malignant phenotype of colorectal cancer cell line HCT116 via inhibiting PI3K/AKT signaling in vitro

Chen

Peng

et al. 2022

Acta Cir. Bras.

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Purpose: Colorectal cancer (CRC) is a common human cancer along with higher incidence and mortality, and this study aimed to identify the effect of cincumol on CRC and its potential mechanisms. Methods: CRC cell line HCT116 was used as the material. Cell proliferation was evaluated by CCK-8 assay, and cell migration was detected by scratch test and Transwell assay. TUNEL staining assay was used to evaluate cell apoptosis. The expression of target genes was detected by qualitative real-time polymerase chain reaction and western blot assays. Results: Cincumol significantly reduced the proliferative and migratory rate and enhanced apoptotic rate of HCT116 cells. Meanwhile, the elevated levels of RBUsuh, Nicd and Tace was also observed in cincumol-treated HCT116 cells. Moreover, our findings revealed that additional cincumol inhibited the expression of p-PI3K and p-AKT, suggesting the inhibition of PI3K/AKT signaling might be involved in the protective role of cincumol on the malignant phenotypes of CRC cells in vitro . Conclusions: Cincumol inhibited the malignant phenotypes of CRC cells in vitro through inactivating PI3K/AKT signaling, suggesting that cincumol might be a potential anti-CRC agent.

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Triazol: A Privileged Scaffold for Proteolysis Targeting Chimeras

Xia

Liu

et al. 2019

Future Med. Chem.

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Current traditional drugs such as enzyme inhibitors and receptor agonists/antagonists present inherent limitations due to occupancy-driven pharmacology as the mode of action. Proteolysis targeting chimeras (PROTACs) are composed of an E3 ligand, a connecting linker and a target protein ligand, and are an attractive approach to specifically knockdown-targeted proteins utilizing an event-driven mode of action. The length, hydrophilicity and rigidity of connecting linkers play important role in creating a successful PROTAC. Some PROTACs with a triazole linker have displayed promising anticancer activity. This review provides an overview of PROTACs with a triazole scaffold and discusses its structure–activity relationship. Important milestones in the development of PROTACs are addressed and a critical analysis of this drug discovery strategy is also presented.

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Emerging Drugs in Refractory Colorectal Cancer

Cited by 3 publications

References 33 publications

Suppressing the secretion of exosomal miR-19b by gw4869 could regulate oxaliplatin sensitivity in colorectal cancer

Suppressing the secretion of exosomal miR-19b by gw4869 could regulate oxaliplatin sensitivity in colorectal cancer

Cincumol prevents malignant phenotype of colorectal cancer cell line HCT116 via inhibiting PI3K/AKT signaling in vitro

Triazol: A Privileged Scaffold for Proteolysis Targeting Chimeras

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