Vitamin B1 suppresses liver cancer growth and restores tumor microcirculation.
Аннотация
Inadequate perfusion and hypoxia constitute the primary characteristics of tumor vasculature and drive malignant progression. Strategies aiming at alleviating hypoxia and enhancing blood perfusion may potentiate chemotherapy and immunotherapy, thereby restraining tumor growth. Vitamin B1 (VitB1), an essential coenzyme for multiple metabolic enzymes, plays a crucial role in cellular energy metabolism and in maintaining the balance between glycolysis and the tricarboxylic acid cycle. However, whether the tumor-suppressive effects of VitB1 are associated with modulation of tumor microcirculation remains unclear. This study aimed to evaluate the anti-tumor effects of VitB1 and to investigate the potential relationship with microcirculatory changes in liver cancer. VitB1 inhibited tumor-cell proliferation in vitro, indicating a potential direct effect on tumor cells. In vivo, VitB1 suppressed liver cancer growth in a dose-dependent manner. High- and medium-dose VitB1 treatment increased microvascular blood perfusion and flow velocity assessed using a laser Doppler flowmetry (LDF) system and decreased tumor microvessel density, without affecting tumor microvascular red blood cell concentration. Moreover, high- and medium-dose VitB1 significantly increased the amplitudes of the neurogenic and endothelial oscillatory components of blood perfusion and flow velocity. These findings suggest that the anti-tumor effects of VitB1 may involve the modulation of neurogenic and endothelial activity, which is associated with improved tumor microhemodynamics. Further studies are needed to elucidate the precise mechanisms and the interplay between direct tumor cell effects and microcirculatory changes.
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.