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1.
Potential therapeutic effects of curcumin in gastric cancer.
Barati, N, Momtazi-Borojeni, AA, Majeed, M, Sahebkar, A
Journal of cellular physiology. 2019;(3):2317-2328
Abstract
Despite recent advancements in understanding of the biology of gastric cancer, treatment of patients with advanced gastric cancer remains a major problem. Among different type of phytochemicals, curcumin, a welltable -known phytochemical, has been shown to be a promising cancer chemopreventive agent. Pharmacokinetics, safety, and efficacy of curcumin have been evaluated in several clinical trials against numerous diseases, and for the treatment of human cancer. In the present review, we have collected in vitro and in vivo investigations and studied the chemosensitizing and anticancer effects of curcumin against the gastric cancer cells. In summary, curcumin has been found to have efficient chemosensitizing effect and also inhibits viability, proliferation, and migration of gastric cancer cells mainly via cell cycle arrest and induction of apoptosis by both mitochondrial-dependent and -independent pathways.
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2.
The latest progress on miR-374 and its functional implications in physiological and pathological processes.
Bian, H, Zhou, Y, Zhou, D, Zhang, Y, Shang, D, Qi, J
Journal of cellular and molecular medicine. 2019;(5):3063-3076
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Abstract
Non-coding RNAs (ncRNAs) have been emerging players in cell development, differentiation, proliferation and apoptosis. Based on their differences in length and structure, they are subdivided into several categories including long non-coding RNAs (lncRNAs >200nt), stable non-coding RNAs (60-300nt), microRNAs (miRs or miRNAs, 18-24nt), circular RNAs, piwi-interacting RNAs (26-31nt) and small interfering RNAs (about 21nt). Therein, miRNAs not only directly regulate gene expression through pairing of nucleotide bases between the miRNA sequence and a specific mRNA that leads to the translational repression or degradation of the target mRNA, but also indirectly affect the function of downstream genes through interactions with lncRNAs and circRNAs. The latest studies have highlighted their importance in physiological and pathological processes. MiR-374 family member are located at the X-chromosome inactivation center. In recent years, numerous researches have uncovered that miR-374 family members play an indispensable regulatory role, such as in reproductive disorders, cell growth and differentiation, calcium handling in the kidney, various cancers and epilepsy. In this review, we mainly focus on the role of miR-374 family members in multiple physiological and pathological processes. More specifically, we also summarize their promising potential as novel prognostic biomarkers and therapeutic targets from bench to bedside.
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3.
Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells.
Akula, SM, Candido, S, Libra, M, Abrams, SL, Steelman, LS, Lertpiriyapong, K, Ramazzotti, G, Ratti, S, Follo, MY, Martelli, AM, et al
Advances in biological regulation. 2019;:100633
Abstract
Pancreatic cancer is devastating cancer worldwide with few if any truly effective therapies. Pancreatic cancer has an increasing incidence and may become the second leading cause of death from cancer. Novel, more effective therapeutic approaches are needed as pancreatic cancer patients usually survive for less than a year after being diagnosed. Control of blood sugar levels by the prescription drug metformin in diseases such as diabetes mellitus has been examined in association with pancreatic cancer. While the clinical trials remain inconclusive, there is hope that certain diets and medications may affect positively the outcomes of patients with pancreatic and other cancers. Other natural compounds may share some of the effects of metformin. One "medicinal" fruit consumed by millions worldwide is berberine (BBR). Metformin and BBR both activate AMP-activated protein kinase (AMPK) which is a key mediator of glucose metabolism. Glucose metabolism has been shown to be very important in cancer and its significance is increasing. In the following studies, we have examined the effects of metformin, BBR and a panel of modified BBRs (NAX compounds) and chemotherapeutic drugs on the growth of four different human pancreatic adenocarcinoma cell lines (PDAC). Interestingly, the effects of metformin could be enhanced by BBR and certain modified BBRs. Upon restoration of WT-TP53 activity in MIA-PaCa-2 cells, an altered sensitivity to the combination of certain NAX compounds and metformin was observed compared to the parental cells which normally lack WT-TP53. Certain NAX compounds may interact with WT-TP53 and metformin treatment to alter the expression of key molecules involved in cell growth. These results suggest a therapeutic approach by combining certain pharmaceutical drugs and nutraceuticals to suppress the growth of cancer cells.
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4.
Gluconeogenesis in cancer cells - Repurposing of a starvation-induced metabolic pathway?
Grasmann, G, Smolle, E, Olschewski, H, Leithner, K
Biochimica et biophysica acta. Reviews on cancer. 2019;(1):24-36
Abstract
Cancer cells constantly face a fluctuating nutrient supply and interference with adaptive responses might be an effective therapeutic approach. It has been discovered that in the absence of glucose, cancer cells can synthesize crucial metabolites by expressing phosphoenolpyruvate carboxykinase (PEPCK, PCK1 or PCK2) using abbreviated forms of gluconeogenesis. Gluconeogenesis, which in essence is the reverse pathway of glycolysis, uses lactate or amino acids to feed biosynthetic pathways branching from glycolysis. PCK1 and PCK2 have been shown to be critical for the growth of certain cancers. In contrast, fructose-1,6-bisphosphatase 1 (FBP1), a downstream gluconeogenesis enzyme, inhibits glycolysis and tumor growth, partly by non-enzymatic mechanisms. This review sheds light on the current knowledge of cancer cell gluconeogenesis and its role in metabolic reprogramming, cancer cell plasticity, and tumor growth.
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5.
Silymarin antiproliferative and apoptotic effects: Insights into its clinical impact in various types of cancer.
Hosseinabadi, T, Lorigooini, Z, Tabarzad, M, Salehi, B, Rodrigues, CF, Martins, N, Sharifi-Rad, J
Phytotherapy research : PTR. 2019;(11):2849-2861
Abstract
Silymarin is a complex extract isolated from the plant Silybum marianum, widely known for its prominent antioxidant and hepatoprotective effects, although increasing evidences have reported extraordinary antiproliferative and apoptotic abilities. As a result, several signaling pathways involved in cell cycle control, cell proliferation, and cell death have been deconvoluted as critical mechanisms. In this regard, cyclin and cyclin-dependent pathways have been the most studied ones. Following that, apoptotic pathways, such as p53, Akt, STAT-3, Ras, and caspases pathways, have been extensively studied, although other mechanisms involved in inflammation and angiogenesis have also been highlighted as silymarin-likely targets in cancer therapy. Therefore, the main challenge of this review is to discuss the diverse molecular mechanisms for silymarin antiproliferative and apoptotic effects; most of them largely studied in various types of cancers so far. Clinical trials and combination therapies related to silymarin application in cancer prevention and treatment are presented as well.
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6.
Potential Anticancer Properties and Mechanisms of Action of Formononetin.
Jiang, D, Rasul, A, Batool, R, Sarfraz, I, Hussain, G, Mateen Tahir, M, Qin, T, Selamoglu, Z, Ali, M, Li, J, et al
BioMed research international. 2019;:5854315
Abstract
Nature, a vast reservoir of pharmacologically active molecules, has been most promising source of drug leads for the cure of various pathological conditions. Formononetin is one of the bioactive isoflavones isolated from different plants mainly from Trifolium pratense, Glycine max, Sophora flavescens, Pycnanthus angolensis, and Astragalus membranaceus. Formononetin has been well-documented for its anti-inflammatory, anticancer, and antioxidant properties. Recently anticancer activity of formononetin is widely studied. This review aims to highlight the pharmacological potential of formononetin, thus providing an insight of its status in cancer therapeutics. Formononetin fights progression of cancer via inducing apoptosis, arresting cell cycle, and halting metastasis via targeting various pathways which are generally modulated in several cancers. Although reported data acclaims various biological properties of formononetin, further experimentation on mechanism of its action, medicinal chemistry studies, and preclinical investigations are surely needed to figure out full array of its pharmacological and biological potential.
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7.
Demethoxycurcumin: A naturally occurring curcumin analogue for treating non-cancerous diseases.
Hatamipour, M, Ramezani, M, Tabassi, SAS, Johnston, TP, Sahebkar, A
Journal of cellular physiology. 2019;(11):19320-19330
Abstract
Turmeric extracts contain three primary compounds, which are commonly referred to as curcuminoids. They are curcumin, demethoxycurcumin (DMC), and bisdemethoxycurcumin. While curcumin has been the most extensively studied of the curcuminoids, it suffers from low overall oral bioavailability due to extremely low absorption as a result of low water solubility and instability at acidic pH, as well as rapid metabolism and clearance from the body. However, DMC, which lacks the methoxy group on the benzene ring of the parent structure, has much greater chemical stability at physiological pH and has been recently reported to exhibit antitumor properties. However, the treatment of noncancerous diseases with DMC has not been comprehensively reviewed. Therefore, here we evaluate published scientific literature on the therapeutic properties of DMC. The beneficial pharmacological actions of DMC include anti-inflammatory, neuroprotective, antihypertensive, antimalarial, antimicrobial, antifungal, and vasodilatory properties. In addition, DMC's ability to ameliorate the effects of free radicals and an environment characterized by oxidative stress caused by the accumulation of advanced glycation end-products associated with diabetic nephropathy, as well as DMC's capacity to inhibit the migration and proliferation of vascular smooth muscle cells following balloon angioplasty are also addressed. This review collates the available literature regarding the therapeutic possibilities of DMC in noncancerous conditions.
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8.
Targeting the death receptor signaling pathway as a potential therapeutic target in the treatment of colorectal cancer.
Moradi Marjaneh, R, Hassanian, SM, Ghobadi, N, Ferns, GA, Karimi, A, Jazayeri, MH, Nasiri, M, Avan, A, Khazaei, M
Journal of cellular physiology. 2018;(10):6538-6549
Abstract
Despite advances in the diagnosis and treatment of colorectal cancer (CRC), it remains a major cause of cancer related death globally. There are currently no chemotherapeutic agents that have been found to eradicate the disease without adverse effects. A defect in the death receptor signaling pathway is a feature of CRC. The ligand of these receptors belongs to the tumor necrosis factor family, and that are particularly expressed by cells of the immune system, and that induce apoptosis in a caspase dependent manner. The fact that malignant cells are particularly sensitive to these ligands, compared to normal cells, has led to work on the assessment of compounds that activate this pathway in the treatment of CRC. Phase I trials have shown that these death receptor agonists are safe. Phase II and III trials are currently investigating the efficacy of these therapeutic agents in the treatment of CRC. In this review, we describe the biochemical death receptor signaling pathway and its relationship to CRC. We also summarize the current clinical studies that are targeting this signaling pathway in CRC treatment.
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9.
CIN-TCP transcription factors: Transiting cell proliferation in plants.
Sarvepalli, K, Nath, U
IUBMB life. 2018;(8):718-731
Abstract
Leaves are the most conspicuous planar organs in plants, designed for efficient capture of sunlight and its conversion to energy that is channeled into sustaining the entire biosphere. How a few founder cells derived from the shoot apical meristem give rise to diverse leaf forms has interested naturalists and developmental biologists alike. At the heart of leaf morphogenesis lie two simple cellular processes, division and expansion, that are spatially and temporally segregated in a developing leaf. In leaves of dicot model species, cell division occurs predominantly at the base, concomitant with the expansion and differentiation of cells at the tip of the lamina that drives increase in leaf surface area. The timing of the transition from one cell fate (division) to the other (expansion) within a growing leaf lamina is a critical determinant of final leaf shape, size, complexity and flatness. The TCP proteins, unique to plant kingdom, are sequence-specific DNA-binding transcription factors that control several developmental and physiological traits. A sub-group of class II TCPs, called CINCINNATA-like TCPs (CIN-TCPs henceforth), are key regulators of the timing of the transition from division to expansion in dicot leaves. The current review highlights recent advances in our understanding of how the pattern of CIN-TCP activity is translated to the dynamic spatio-temporal control of cell-fate transition through the transactivation of cell-cycle regulators, growth-repressing microRNAs, and interactions with the chromatin remodeling machinery to modulate phytohormone responses. Unravelling how environmental inputs influence CIN-TCP-mediated growth control is a challenge for future studies. © 2018 IUBMB Life, 70(8):718-731, 2018.
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10.
Demethoxycurcumin: A naturally occurring curcumin analogue with antitumor properties.
Hatamipour, M, Ramezani, M, Tabassi, SAS, Johnston, TP, Ramezani, M, Sahebkar, A
Journal of cellular physiology. 2018;(12):9247-9260
Abstract
The eradication of cancer in a patient remains an elusive challenge despite advances in early detection and diagnosis, chemo- and immunotherapy, pinpoint radiation treatments, and expert surgical intervention. Although significant gains have been made in our understanding of cancer cell biology, a definite cure for most cancers does not exist at present. Thus, it is not surprising that the research and medical communities continue to explore the importance and therapeutic potential of natural products in their multimodality cancer treatment approach. Curcuminoids found in turmeric are one such class of natural products that have been extensively investigated for their potential to halt the progression of cancer cell proliferation and, more important, to stop metastasis from occurring. In this review, we examine one curcuminoid (demethoxycurcumin [DMC]) largely because of its increased stability and better aqueous solubility at physiological pH, unlike the more well-known curcuminoid (curcumin), which is largely unabsorbed after oral ingestion. The present review will focus on the signaling pathways that DMC utilizes to modulate the growth, invasion, and metastasis of cancer cells in an effort to provide enhanced mechanistic insight into DMC's action as it pertains to brain, ovarian, breast, lung, skin, and prostate cancer. Additionally, this review will attempt to provide an overview of DMC's mechanism of action by modulating apoptosis, cell cycle, angiogenesis, metastasis, and chemosensitivity. Lastly, it is hoped that increased understanding will be gained concerning DMC's interactive role with microRNA-551a, 5' adenosine monophosphate-activated protein kinase, nuclear factor-κB, Wnt inhibitory factor-1, and heat shock protein 70 to affect the progression of cancer.