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Combination of azacytidine and curcumin is a potential alternative in decitabine-resistant colorectal cancer cells with attenuated deoxycytidine kinase
Biochem Biophys Res Commun. 2021 Sep 22;578:157-162. doi: 10.1016/j.bbrc.2021.09.041. Online ahead of print.ABSTRACTDecitabine (DAC), a DNA methyltransferase (DNMT) inhibitor is a novel anti-cancer drug regulating epigenetic mechanisms. Similar to conventional anti-cancer drugs, drug resistance to DAC also has been reported, resulting in tumor recurrence. Our previous study using colorectal cancer HCT116 cells found the decrease in deoxycytidine kinase (dCK) (activation enzyme of DAC) and the increase in cytidine deaminase (inactivation enzyme of DAC) in acquired DAC-resistant HCT116 (HCT116/DAC) cells. The aim of our stud...
Source: Biochemical and Biophysical Research communications - September 27, 2021 Category: Biochemistry Authors: Mika Hosokawa Risako Seiki Seigo Iwakawa Ken-Ichi Ogawara Source Type: research

Myeloid Derived Suppressor Cells Interactions With Natural Killer Cells and Pro-angiogenic Activities: Roles in Tumor Progression
Conclusions MDSC are major players in the immunosuppressive scenario in cancer, thanks to their phenotype heterogeneity and critical interaction with several innate immune cells, thus representing a crucial target in oncology. Here we reviewed the interactions of MDSCs with NK cells. The contribution of key cytokines, chemokines and mediators active in this process have been discussed. We also described the contribution of MDSC on angiogenesis directly or indirectly through interactions with NK and immunosuppressive activities. A parallel of the cancer associated to the decidual counterpart of these cells is discussed, a...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Sanguinarine Induces Apoptosis Pathway in Multiple Myeloma Cell Lines via Inhibition of the JaK2/STAT3 Signaling
In this study, we aimed to investigate the potential anti-proliferative and pro-apoptotic activities of SNG in a panel of MM cell lines (U266, IM9, MM1S, and RPMI-8226). SNG treatment of MM cells resulted in a dose-dependent decrease in cell viability through mitochondrial membrane potential loss and activation of caspase 3, 9, and cleavage of PARP. Pre-treatment of MM cells with a universal caspase inhibitor, Z-VAD-FMK, prevented SNG mediated loss of cell viability, apoptosis, and caspase activation, confirming that SNG-mediated apoptosis is caspase-dependent. The SNG-mediated apoptosis appears to be resulted from suppres...
Source: Frontiers in Oncology - April 16, 2019 Category: Cancer & Oncology Source Type: research

Curcumin inhibits tumor epithelial‑mesenchymal transition by downregulating the Wnt signaling pathway and upregulating NKD2 expression in colon cancer cells.
Authors: Zhang Z, Chen H, Xu C, Song L, Huang L, Lai Y, Wang Y, Chen H, Gu D, Ren L, Yao Q Abstract Tumor invasion and metastasis are closely associated with epithelial‑mesenchymal transition (EMT). EMT refers to epithelial cells under physiological and pathological conditions that are specific to mesenchymal transition. Curcumin inhibits EMT progression via Wnt signaling. The Wnt signaling pathway is a conservative EMT‑related signaling pathway that is involved in the development of various tumors. In the present study, MTS assays were employed to analyze the proliferation of curcumin‑treated cells. Naked c...
Source: Oncology Reports - March 19, 2016 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

GADD45α modulates curcumin sensitivity through c-Abl- and JNK-dependent signaling pathways in a mismatch repair-dependent manner.
In this report, we show that the protein levels of gadd45α, whose transcript levels are increased during DNA damage and stress signals, are upregulated following curcumin treatment in a dose- and time-dependent manner. We further observed that cells compromised for Mlh1 function (HCT116 + Ch2) displayed ~twofold increased GADD45α upregulation compared to similarly treated proficient counterparts (HCT116 + Ch3). Similarly, suppression of Mlh1 using ShRNA increased GADD45α upregulation upon curcumin treatment. On the other hand, suppression of GADD45α using SiRNA-blocked curcumin-induced cell death induction in Mlh1-...
Source: Molecular and Cellular Biochemistry - January 30, 2016 Category: Biochemistry Authors: Naick H, Jin S, Baskaran R Tags: Mol Cell Biochem Source Type: research

Abstract 3903: A sub-set of DCLK1+ve colon cancer stem cells (CSCs) survive curcumin induced autophagy, while co-treatment with curcumin +DCLK1-siRNA eliminates CSCs: Role of long and short isofoms of DCLK1
Conclusion. Our studies strongly suggest that, 1) DCLK1 represents a functional protein for colon cancers, 2) combination of curcumin+DCLK1-siRNA may target and eradicate colon cancer stem cells., and 3) identifying small molecules that inhibit expression of S-isoform may allow to specifically target cancer stem cells, while sparing normal stem cells for cancer treatment purposes. This work was supported by NIH Granst to PS (R01CA09795909 and RO1CA0975909-S1). Citation Format: Shubhashish Sarkar, Malaney O'Connell, Carla, Kantara, Pomila Singh. A sub-set of DCLK1+ve colon cancer stem cells (CSCs) survive curcumin induced a...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Sarkar, S., O'Connell, M., Kantara, C., Singh, P. Tags: Tumor Biology Source Type: research

Abstract 2283: Potent curcumin analog FLLL-12 targets both intrinsic and extrinsic signaling pathways to induce apoptosis in lung cancers
Conclusions: Our results strongly suggest that FLLL-12 is a potent curcumin analog that induces apoptosis of lung cancer cell lines by targeting: (1) intrinsic pathways via transcriptional inhibition of EGFR and AKT and induction of BIM, and (2) extrinsic pathway via induction of DR5. Future in vivo studies using appropriate animal models are warranted for further development of this promising compound for cancer prevention and/or treatment for lung cancer. (Supported by R03CA171663, P50CA128613 and Robbins Scholar Award of Winship Cancer Institute of Emory University). Citation Format: A.R.M. Ruhul Amin, Abedul Haque, Moh...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Amin, A. R. M. R., Haque, A., Rahman, M. A., Fuchs, J. R., Chen, Z. G., Shin, D. M. Tags: Molecular and Cellular Biology Source Type: research