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Liver cancer is one of the leading cancers, especially in developing countries. Understanding the biomechanical properties of the liver cancer cells can not only help to elucidate the mechanisms behind the cancer progression, but also provide important information for diagnosis and treatment. At the cellular level, we used well-established atomic force microscopy (AFM) techniques to characterize the heterogeneity of mechanical properties of two different types of human liver cancer cells and a normal liver cell line. Stiffness maps with a resolution of 128x128 were acquired for each cell. The distributions of the indentation moduli of the cells showed significant differences between cancerous cells and healthy controls. Significantly, the variability was even greater amongst different types of cancerous cells. Fitting of the histogram of the effective moduli using a normal distribution function showed the Bel7402 cells were stiffer than the normal cells while HepG2 cells were softer. Morphological analysis of the cell structures also showed a higher cytoskeleton content among the cancerous cells. Results provided a foundation for applying knowledge of cell stiffness heterogeneity to search for tissue-level, early-stage indicators of liver cancer.
Cancer cells usually utilize glucose as a carbon source for aerobic glycolysis, a phenomenon known as the Warburg effect. And a high rate of glycolysis has been observed in lung cancer cells. The growing evidence indicates that long non-coding RNAs (lncRNAs) are important players in lung cancer initiation and progression. However, the correlation between lncRNAs and glycolysis remains unclear. In this study, we recognized a lncRNA, LNC CRYBG3, which can interact with lactate dehydrogenase A (LDHA), a vital enzyme of glycolysis, is highly upregulated in both clinical lung cancer tissues and in vitro cultured lung cancer cell lines. A positive correlation between the expression level of LNC CRYBG3 and LDHA expression levels is observed. In another hand, LNC CRYBG3 is a regulator of glycolysis and its overexpression promoted the uptake of glucose and the production of lactate whereas the knockdown of LNC CRYBG3 led to opposite results and suppressed cell proliferation. These results indicated that LNC CRYBG3 might be a novel target for lung cancer treatment.
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