Metabolic reprogramming in tumor immune microenvironment: Impact on immune cell function and therapeutic implications.

Understanding of the metabolic reprogramming has revolutionized our insights into tumor progression and potential treatment. This review concentrates on the aberrant metabolic pathways in cancer cells within the tumor microenvironment (TME). Cancer cells differ from normal cells in their metabolic processing of glucose, amino acids, and lipids in order to adapt to heightened biosynthetic and energy needs. These metabolic shifts, which crucially alter lactic acid, amino acid and lipid metabolism, affect not only tumor cell proliferation but also TME dynamics. This review also explores the reprogramming of various immune cells in the TME. From a therapeutic standpoint, targeting these metabolic alterations represents a novel cancer treatment strategy. This review also discusses approaches targeting the regulation of metabolism of different nutrients in tumor cells and influencing the tumor microenvironment to enhance the immune response. In summary, this review summarizes metabolic reprogramming in cancer and its potential as a target for innovative therapeutic strategies, offering fresh perspectives on cancer treatment.

Radiation Protection of Polydatin Against Radon Exposure Injury of Epithelial Cells and Mice.

Radon exposure is significantly associated with lung cancer. Radon concentration is currently reduced mainly by physical methods, but there is a lack of protective drugs or biochemical reagents for radon damage. This study aimed to explore the protective effect of polydatin (PD) on the radon-exposed injury. The results showed that PD can significantly reduce ROS level, raise SOD activity, weaken the migration ability, increase E-cad, and decrease mesenchymal cell surface markers (FN1, Vimentin, N-cad, α-SMA, and Snail) in radon-exposed epithelial cells. In vivo, PD increased the mice weight, promoted SOD activity, and decreased MDA content, the number of bullae, pulmonary septum thickness, lung collagenous fibers, and mesenchymal cell surface markers. Furthermore, PD inhibited p-PI3K, p-AKT, and p-mTOR expression. Compared with directly adding PD on radon-exposed cells, adding PD before and after radon exposure could more obviously improve the adhesion of radon-exposed cells, significantly alleviate the migration ability, and more significantly reduce mesenchyme markers and p-AKT and p-mTOR. These results indicate that PD can reduce oxidative stress, weaken epithelial-mesenchymal transition (EMT) and lung fibrosis in radon-exposed cells/mice, and have good radiation protection against radon injury. The mechanism is related to the inhibition of the PI3K/AKT/mTOR pathway.

miR­30a inhibits epithelial­mesenchymal transition and metastasis in triple­negative breast cancer by targeting ROR1.

Triple­negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. In the present study, we revealed that the expression of miR­30a was significantly decreased in TNBC, and TNBC patients with low expression of miR­30a were associated with high histological grade and more lymph node metastasis. Moreover, we found that miR­30a suppressed TNBC cell epithelial­mesenchymal transition (EMT), as demonstrated by the overexpression of miR­30a which increased the expression of epithelial marker E­cadherin but decreased the expression of mesenchymal markers N­cadherin and vimentin. Furthermore, we demonstrated that overexpression of miR­30a significantly suppressed TNBC cell invasion and migration, as well as inhibited tumor growth and metastasis in vivo. More importantly, RTK­like orphan receptor 1 (ROR1) was predicted as the direct target of miR­30a, which was subsequently confirmed by luciferase assays. Forced expression of miR­30a in TNBC cells decreased ROR1 expression, whereas the overexpression of ROR1 reversed the suppressive effects of miR­30a in TNBC cell migration and invasion. Collectively, this study indicated that miR­30a functions as a tumor­metastasis suppressor miRNA in TNBC by directly targeting ROR1 and that miR­30a may serve as a novel therapeutic target for TNBC.

[Efficacy of hypofractionated radiotherapy combined with docetaxel for treatment of bone metastasis of lung cancer].

OBJECTIVE: To evaluate the efficacy of hypofractionated radiotherapy combined with docetaxel for treatment of bone metastasis of lung cancer and explore the factors related to the prognosis. METHODS: Seventy-two patients with bone metastasis of lung cancer were divided into group A with hypofractionated radiotherapy at 3.0 Gy /fraction (once a day, 5 days per week for 30 Gy) and weekly docetaxel treatment at 60 mg for 2 weeks, and group B with radiotherapy alone at 2.0 Gy/fraction (once a day, 5 days per week for 40 Gy). RESULTS: The total effective rate was 93.1% (67/72) in these patients, with a non-response rate of 6.9% (5/72). The total effective rate was 97.2% (35/36) in group A and 88.9% (32/36) in group B. After the radiotherapy, the analgesic effect showed no significant difference between the two groups, but the onset of the effect was faster in group B than in group A. CONCLUSION: Local radiotherapy provides effective pain relief in patients with bone metastasis of lung cancer. High-dose fractionated irradiation can rapidly achieve the analgesic effect.

[Radiotherapy with concurrent chemotherapy for treatment of advanced nasopharyngeal carcinoma].

OBJECTIVE: To evaluate the effect of radiotherapy combined with concurrent chemotherapy for the treatment of advanced nasopharyngeal carcinoma. METHODS: From February 2001 to August 2003, 80 cases of nasopharyngeal carcinoma (stage III and IVa) were randomized into two groups to receive radiotherapy with concurrent chemotherapy (Group A, n=40) consisted of leucovorin (CF, 100 mg/m(2), days 1-5), 5-fluorouracil (5-Fu, 500 mg/m(2), days 1-5), cisplatin (DDP, 60 mg/m(2), day 1) for one course followed by another 4 weeks later, or radiotherapy alone (Group B, n=40). In all cases, the radiotherapy followed the same protocol, with the nasopharyngeal (NP) total dose (DT) of 66-76 Gy given in 6.6-7.6 weeks, and cervical lymphnode (LN) DT of 60-72 Gy completed in 6.0-7.2 weeks. RESULTS: All patients completed the treatment course, and the complete response rates of the primary lesions and cervical nodes in A and B groups were 77.5% and 60.0% (P>0.05) and 92.5% vs 70.0% (P<0.05), respectively, which were 92.5% vs 72.5% (P<0.05) and 100% vs 85.0% (P<0.05), respectively, 3 months after treatment. No obvious toxicity was observed in the two groups except for vomiting and leukopenia. CONCLUSION: Radiotherapy with concurrent chemotherapy can improve the elimination rate of advanced nasopharyngeal carcinoma, and can be completed in shorter treatment course in comparison with neoadjuvant chemotherapy before radiotherapy, eligible for clinical practice in the treatment of advanced nasopharyngeal carcinoma.