Effect of color cross-correlated noise on the growth characteristics of tumor cells under immune surveillance

Based on the Michaelis-Menten reaction model with catalytic effects, a more comprehensive one-dimensional stochastic Langevin equation with immune surveillance for a tumor cell growth system is obtained by considering the fluctuations in growth rate and mortality rate. To explore the impact of environmental fluctuations on the growth of tumor cells, the analytical solution of the steady-state probability distribution function of the system is derived using the Liouville equation and Novikov theory, and the influence of noise intensity and correlation intensity on the steady-state probability distributional function are discussed. The results show that the three extreme values of the steady-state probability distribution function exhibit a structure of two peaks and one valley. Variations of the noise intensity, cross-correlation intensity and correlation time can modulate the probability distribution of the number of tumor cells, which provides theoretical guidance for determining treatment plans in clinical treatment. Furthermore, the increase of noise intensity will inhibit the growth of tumor cells when the number of tumor cells is relatively small, while the increase in noise intensity will further promote the growth of tumor cells when the number of tumor cells is relatively large. The color cross-correlated strength and cross-correlated time between noise also have a certain impact on tumor cell proliferation. The results help people understand the growth kinetics of tumor cells, which can a provide theoretical basis for clinical research on tumor cell growth

The microprotein encoded by exosomal lncAKR1C2 promotes gastric cancer lymph node metastasis by regulating fatty acid metabolism

Abstract Lymph node metastasis (LNM) is the prominent route of gastric cancer dissemination, and usually leads to tumor progression and a dismal prognosis of gastric cancer. Although exosomal lncRNAs have been reported to be involved in tumor development, whether secreted lncRNAs can encode peptides in recipient cells remains unknown. Here, we identified an exosomal lncRNA (lncAKR1C2) that was clinically correlated with lymph node metastasis in gastric cancer in a VEGFC-independent manner. Exo-lncAKR1C2 secreted from gastric cancer cells was demonstrated to enhance tube formation and migration of lymphatic endothelial cells, and facilitate lymphangiogenesis and lymphatic metastasis in vivo. By comparing the metabolic characteristics of LN metastases and primary focuses, we found that LN metastases of gastric cancer displayed higher lipid metabolic activity. Moreover, exo-lncAKR1C2 encodes a microprotein (pep-AKR1C2) in lymphatic endothelial cells and promotes CPT1A expression by regulating YAP phosphorylation, leading to enhanced fatty acid oxidation (FAO) and ATP production. These findings highlight a novel mechanism of LNM and suggest that the microprotein encoded by exosomal lncAKR1C2 serves as a therapeutic target for advanced gastric cancer