Nanoliposomal formulation encapsulating celecoxib and genistein inhibiting COX-2 pathway and Glut-1 receptors to prevent prostate cancer cell proliferation

Tian, Jingyan; Guo, Fengjun; Chen, Yingying; Li, Yanqing; Yu, Bingbing; Li, Yang

doi:10.1016/j.canlet.2019.01.002

Cited by 40 publications

(21 citation statements)

References 49 publications

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“…The occurrence and development of tumors is the result of tumor cell proliferation, apoptosis, and migration, which are affected by multiple conditions. The antiproliferation, proapoptosis, and antimigration effects of celecoxib have been reported in a variety of tumor cells (Jendrossek, 2013;Tai et al, 2019;Tian et al, 2019). Metformin has also been reported to slightly inhibit tumor cell growth (Cheng et al, 2019;Lee et al, 2019), which is consistent with the data in this study.…”

Section: A B D E Fsupporting

confidence: 92%

Metformin Synergistically Enhanced the Antitumor Activity of Celecoxib in Human Non-Small Cell Lung Cancer Cells

Cao

Liu

et al. 2020

Front. Pharmacol.

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Celecoxib has potential as an effective antineoplastic agent, but it may exhibit side effects. Given the glucose-addicted properties of tumor cells, metformin is recognized for its inhibitory effect on oxidative phosphorylation. In the present study, we aimed to combine low dose of celecoxib with metformin to alleviate the side effects of nonsteroidal antiinflammatory drugs (NSAIDs) and overcome potential drug resistance. We found that celecoxib combined with metformin obviously suppressed cell migration and proliferation and induced cell apoptosis. Most importantly, in vivo experiments revealed the superior antitumor efficacy of combination treatment with a low dosage of celecoxib (25 mg/kg/ day) without apparent toxicity. Further study of the underlying mechanism revealed that the two drugs in combination caused ROS aggregation in NSCLC cells, leading to DNA double-strand breaks and increased expression of the tumor suppressor factor p53. Elevated p53 subsequently caused cell cycle arrest and cell proliferation inhibition. The presence of metformin also sensitized NSCLC cells to celecoxib-induced apoptosis by activating caspase-9,-8,-3, and-7, upregulating the pro-apoptotic proteins Bad and Bax, and downregulating the antiapoptotic proteins Bcl-xl and Bcl-2. Moreover, the superior anticancer effect of combined therapy was also due to suppression of Raf-MEK-ERK cascades and PI3K-AKT signaling, which is conducive to overcoming drug resistance. In addition, either celecoxib alone or in combination with metformin suppressed NSCLC cell migration and invasion by inhibiting FAK, N-cadherin, and matrix metalloproteinase-9 activities. Together, our study provided a rational combination strategy with a low dosage of celecoxib and metformin for preclinical cancer application.

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Section: A B D E Fsupporting

confidence: 92%

Metformin Synergistically Enhanced the Antitumor Activity of Celecoxib in Human Non-Small Cell Lung Cancer Cells

Cao

Liu

et al. 2020

Front. Pharmacol.

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“…These molecules are overexpressed in cancer cells; therefore, their inhibition can be a therapeutic strategy against cancer (20,21). The use of compounds that suppress the growth of cancer cells through inhibition of glucose transporters has been widely explored in various types of cancer, including liver, colon, ovary, prostate, brain, and breast cancer (21)(22)(23)(24)(25)(26). For example, in ovarian cancer cells, GLUT-1 and GLUT-3 protein levels are increased 6.5 and 4.1 times, respectively, and a GLUT-1/-3 inhibitor prevents cell growth, targets metabolic plasticity, and overcomes the cellular rescue mechanisms of cancer cells (22).…”

Section: Glucose Metabolism and Transporters In Cancer Cellsmentioning

confidence: 99%

Glycosylated Nanoparticles for Cancer-Targeted Drug Delivery

Torres-Pérez

Pedraza-Escalona

et al. 2020

Front. Oncol.

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Nanoparticles (NPs) are novel platforms that can carry both cancer-targeting molecules and drugs to avoid severe side effects due to nonspecific drug delivery in standard chemotherapy treatments. Cancer cells are characterized by abnormal membranes, metabolic changes, the presence of lectin receptors, glucose transporters (GLUT) overexpression, and glycosylation of immune receptors of programmed death on cell surfaces. These characteristics have led to the development of several strategies for cancer therapy, including a large number of carbohydrate-modified NPs, which have become desirable for use in cell-selective drug delivery systems because they increase nanoparticle-cell interactions and uptake of carried drugs. Currently, the potential of NP glycosylation to enhance the safety and efficacy of carried therapeutic antitumor agents has been widely acknowledged, and much information is accumulating in this field. This review seeks to highlight recent advances in NP stabilization, toxicity reduction, and pharmacokinetic improvement and the promising potential of NP glycosylation from the perspective of molecular mechanisms described for drug delivery systems for cancer therapy. From preclinical proof-of-concept to demonstration of therapeutic value in the clinic, the challenges and opportunities presented by glycosylated NPs, with a focus on their applicability in the development of nanodrugs, are discussed in this review.

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“…GLUT1 is overexpressed in PCa cases in association with Gleason scores, and its action plays a relevant role in enhancing cell proliferation 54–56 . Accordingly, GLUT1 inhibition enhanced the production of reactive oxygen species and induced apoptosis of PCa cells 57 . Nevertheless, both GLUT1 and GLUT3, the high‐affinity GLUTs, as well as GLUT12, have been associated with the increased glucose uptake and glycolytic activity of PCa cells 13,20,58,59 .…”

Section: Bioenergetics Sources and Their Relevance In Pcamentioning

confidence: 99%

Revisiting prostate cancer metabolism: From metabolites to disease and therapy

Cardoso

Carvalho

Fonseca

et al. 2020

Medicinal Research Reviews

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Prostate cancer (PCa), one of the most commonly diagnosed cancers worldwide, still presents important unmet clinical needs concerning treatment. In the last years, the metabolic reprogramming and the specificities of tumor cells emerged as an exciting field for cancer therapy. The unique features of PCa cells metabolism, and the activation of specific metabolic pathways, propelled the use of metabolic inhibitors for treatment. The present work revises the knowledge of PCa metabolism and the metabolic alterations that underlie the development and progression of the disease. A focus is given to the role of bioenergetic sources, namely, glucose, lipids, and glutamine sustaining PCa cell survival and growth. Moreover, it is described as the action of oncogenes/tumor suppressors and sex steroid hormones in the metabolic reprogramming of PCa. Finally, the status of PCa treatment based on the inhibition of metabolic pathways is presented. Globally, this review updates the landscape of PCa metabolism, highlighting the critical metabolic alterations that could have a clinical and therapeutic interest.

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Nanoliposomal formulation encapsulating celecoxib and genistein inhibiting COX-2 pathway and Glut-1 receptors to prevent prostate cancer cell proliferation

Cited by 40 publications

References 49 publications

Metformin Synergistically Enhanced the Antitumor Activity of Celecoxib in Human Non-Small Cell Lung Cancer Cells

Metformin Synergistically Enhanced the Antitumor Activity of Celecoxib in Human Non-Small Cell Lung Cancer Cells

Glycosylated Nanoparticles for Cancer-Targeted Drug Delivery

Revisiting prostate cancer metabolism: From metabolites to disease and therapy

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