Lung cancer is a leading cause of morbidity and mortality. Previous studies have identified that an improvement in treatment efficacy was achieved using
Endostar; however, the role of
Endostar in
lung cancer remains poorly understood. The present study investigated whether the enhanced antitumor effects of
Endostar in combination with radiation involved changes in the metabolism and microenvironment in
non-small cell lung cancer. A
Lewis lung carcinoma mouse model was used, including the control,
Endostar (ES),
radiotherapy (RT) and
Endostar plus
radiotherapy (ES + RT) groups. The
tumor inhibition rates and growth were described based on changes in
tumor volume. In addition, ultraviolet enzymatic analysis was performed to determine the
lactate level and reverse transcription-polymerase chain reaction was used to measure the
mRNA expression of
lactate dehydrogenase (LDH). A Meph-3 pH meter was used to detect the ranges of
tumor interstitial tissue pH, and immunohistochemical analysis was adopted to examine
hypoxia within the tumor microenvironment. The
tumor inhibition rate of the ES + RT group was significantly higher compared with the other three groups (P<0.05). Following treatment, the
lactate levels decreased in all three treatment groups compared with the control, particularly in the ES + RT group (P<0.05). Reduced LDH expression and hypoxic fraction in the tumor microenvironment were also observed in the ES + RT group (P<0.05). Furthermore, changes from acidic to alkaline pH in the tumor microenvironment were detected in the ES + RT group. The present study suggested that
Endostar is involved in the regulation of metabolism and tumor microenvironment
hypoxia, which may be responsible for the enhanced antitumor effect of
Endostar in combination with
radiotherapy.