Measurement of endogenous free and bound NAD(P)H relative concentrations in living cells isa useful method for monitoring aspects of cellular metabolism, because the NADH∕NAD⁺ reduction-oxidation pair is crucial for electron transfer through the mitochondrial electron transport chain. Variations of free and bound NAD(P)H ratio are also implicated in cellular bioenergetic and biosynthetic metabolic changes accompanying cancer. This study uses two-photon fluorescence lifetime imaging microscopy (FLIM) to investigate metabolic changes in MCF10A premalignant breast cancer cells treated with a range of glycolysis inhibitors: namely, 2 deoxy-D-glucose, oxythiamine, lonidamine, and 4-(chloromethyl) benzoyl chloride, as well as the mitochondrial membrane uncoupling agent carbonyl cyanide m-chlorophenylhydrazone. Through systematic analysis of FLIM data from control and treated cancer cells, we observed that all glycolytic inhibitors apart from lonidamine had a slightly decreased metabolic rate and that the presence of serum in the culture medium generally marginally protected cells from the effect of inhibitors. Direct production of glycolytic L-lactate was also measured in both treated and control cells. The combination of these two techniques gave valuable insights into cell metabolism and indicated that FLIM was more sensitive than traditional biochemical methods, as it directly measured metabolic changes within cells as compared to quantification of lactate secreted by metabolically active cells.

A series of new 3-mercapto-1,2,4-triazoles have been designed, synthesized and their structures were identified by nuclear magnetic resonance (NMR) and Fourier transform infrared (FT-IR) spectrophotometric techniques. The target compounds are designed as analogues for the anti-cancer agent Combretastatin A-4 with different aliphatic side substituents. The synthesized novel heterocyclic compounds were evaluated as anticancer molecules against colon cancer cell line (SW480) using the crystal violet cytotoxicity assay. The results revealed that these compounds have growth inhibitive effect on the cancer cells with different inhibition levels. Compound 5a with -SMe group was found to be the most active one with 77.4% cell growth inhibition and 10 µM IC50 value, it was also found to have relatively low cytotoxicity when tested against Madin-Darby Canine Kidney (MDCK) normal cells line. The levels of the antioxidant total capacity of the synthesized triazoles have been determined by using 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay against ascorbic acid as a reference antioxidant agent at 50 μM. Compound 4 showed highest antioxidant activity with DPPH radical scavenging capacity of 71%.

Although its mechanism of action on cancer cells not well understood, Metformin (Met) is widely used nowadays to improve the anticancer activity of some drugs. Metformin has also been shown to decrease the growth of breast cancer cells and pancreatic cancer in hamsters and delays other types of tumors. The aim of this study was to compare the effects of Cisplatin (Cis) alone and Metformin alone on colon cancer cell line SW480. The results showed that the effect of Metformin on cell proliferation is concentration-dependent. Metformin enhances the proliferation and attachment of colon cancer at lower concentrations. Results showed a significant decrease in cell proliferation and attachment of colon cancer cells after Cisplatin treatment.Results of this study revealed that Cisplatin treatment decreased both proliferation and cell adhesion to the matrix. Combination therapy (Met+Cis) showed promising synergism and enhancement of anticancer activity of Cisplatin on colon cancer cells. We are strongly recommended more investigations to be more specific for using Metformin as general anticancer.

Cancers are a group of diseases characterized by uncontrolled growth and the spread of abnormal cells . Colon cancer (CC) is one of the most aggressive tumor that leading to death in the world In this study, an attempt was made to evaluate the effect of different combinations of 2-deoxy-d-glucose, metformin, and doxorubicin on colon cancer cells viability. Results revealed a significant decrease in colon cancer viability after the treatment with combinations of (2-DG- metformin, 2-DG – Dox , and 2-DG- metformin - Dox) at certain concentrations.

Colorectal cancer is one of the most common malignancies in the world. Clinical evidence suggests that non-steroidal anti-inflammatory drugs (NSAIDs ) were found to reduce the risk of colonic adenoma and colorectal cancer occurrence or recurrence and are more beneficial in acute inflammatory disorders than in chronic inflammatory diseases, implying that NSAIDs target the early stages of the inflammatory response. Celecoxib inhibits tumor initiation and tumor cell proliferation. Aspirin inhibits the constitutive isoform of the platelet enzyme cyclooxygenase- 1 (COX-1) and the inducible isoform cyclooxygenase-2 (COX-2) which is expressed by cytokines, and some growth factors. In this study, different concentrations of both Celecoxib and Aspirin in various sets were applied to investigate their effects on colon cancer cells (SW480) proliferation and cytokines production. Our result reported a significant decrease in cells viability after the treatment with aspirin and celecoxib alone or in combination. Celecoxib significantly decreased IL-6 levels, while Aspirin treatment showed no significant change in IL-6, IL-12, and TNF- α levels. In conclusion, non-steroidal anti-inflammatory drugs (NSAIDs) have pronounced anti-proliferative effects on colorectal cancer cell lines.