Mammalian target of rapamycin (mTOR) regulates cell proliferation, autophagy, and apoptosis by participating in multiple signaling pathways in the body. Studies have shown that the mTOR signaling pathway is also associated with cancer, arthritis, insulin resistance, osteoporosis, and other diseases. The mTOR signaling pathway, which is often activated in tumors, not only regulates gene transcription and protein synthesis to regulate cell proliferation and immune cell differentiation but also plays an important role in tumor metabolism. Therefore, the mTOR signaling pathway is a hot target in anti-tumor therapy research. In recent years, a variety of newly discovered mTOR inhibitors have entered clinical studies, and a variety of drugs have been proven to have high activity in combination with mTOR inhibitors. The purpose of this review is to introduce the role of mTOR signaling pathway on apoptosis, autophagy, growth, and metabolism of tumor cells, and to introduce the research progress of mTOR inhibitors in the tumor field.

Cancer immunotherapy is an innovative treatment for tumors today. In various experiments and clinical studies, it has been found that immunotherapy does have incomparable advantages over traditional anti-tumor therapy, which can prolong progression-free survival (PFS) and overall survival (OS). However, immunotherapy has obvious complexity and uncertainty. Immunotherapy may also cause severe adverse reactions due to an overactive immune system. More effective and fewer adverse reactions immunological checkpoints are still under further exploration. This review gives an overview of recent developments in immunotherapy and indicates a new direction of tumor treatment through analyzing the pros and cons of immunotherapy coupled with keeping a close watch on the development trend of the immunotherapy future.

The patients with high microsatellite instability (MSI-H)/mismatch repair deficient (dMMR) tumors recently have been reported that can benefit from immunotherapy, and MSI can be used as a genetic instability of a tumor detection index. However, many studies have shown that there are many heterogeneous phenomena in patients with MSI tumors in terms of immunotherapy, prognosis and chemotherapy sensitivity. Here we mainly review the research results of MSI detection methods, the mechanisms of MSI occurrence and its relationship with related tumors, aiming to make a brief analysis of the current research status of MSI and provide comparable reference and guidance value for further research in this field.

Single-cell sequencing technologies can be used to detect the genome, transcriptome and other multi-omics of single cells. They can show the differences and evolutionary relationships of various cells. This review introduces the latest advances in single-cell sequencing technologies and their applications in oncology, microbiology, neurology, reproduction, immunology, digestive and urinary systems, highlighting the important role that single-cell sequencing techniques play in these areas.

Lung cancer is one of the common malignant tumors that threaten human life with serious incidence and high mortality. According to the histopathological characteristics, lung cancer is mainly divided into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). NSCLC accounts for about 80-85% of lung cancers. In fact, lung cancer metastasis is a major cause of treatment failure in clinical patients. The underlying reason is that the mechanisms of lung cancer metastasis are still not fully understood. The metastasis of lung cancer cells is controlled by many factors, including the interaction of various components in the lung cancer microenvironment, epithelial-mesenchymal transition (EMT) transformation, and metastasis of cancer cells through blood vessels and lymphatics. The molecular relationships are even more intricate. Further study on the mechanisms of lung cancer metastasis and in search of effective therapeutic targets can bring more reference directions for clinical drug research and development. This paper focuses on the factors affecting lung cancer metastasis and connects with related molecular mechanisms of the lung cancer metastasis and mechanisms of lung cancer to specific organs, which mainly reviews the latest research progress of NSCLC metastasis. Besides, in this paper, experimental models of lung cancer and metastasis, mechanisms in SCLC transfer and the challenges about clinical management of lung cancer are also discussed. The review is intended to provide reference value for the future research in this field and promising treatment clues for clinical patients.

Background: Satellite cells (SCs) are critical to skeletal muscle regeneration. Inactivation of SCs is linked to skeletal muscle loss. Transferrin receptor 1 (Tfr1) is associated with muscular dysfunction as muscle‐specific deletion of Tfr1 results in growth retardation, metabolic disorder, and lethality, shedding light on the importance of Tfr1 in muscle physiology. However, its physiological function regarding skeletal muscle ageing and regeneration remains unexplored. Methods: RNA sequencing is applied to skeletal muscles of different ages to identify Tfr1 associated to skeletal muscle ageing. Mice with conditional SC ablation of Tfr1 were generated. Between Tfr1 ^SC/WT and Tfr1 ^SC/KO ( n = 6–8 mice per group), cardiotoxin was intramuscularly injected, and transverse abdominal muscle was dissected, weighted, and cryosectioned, followed by immunostaining, haematoxylin and eosin staining, and Masson staining. These phenotypical analyses were followed with functional analysis such as flow cytometry, tread mill, Prussian blue staining, and transmission electron microscopy to identify pathological pathways that contribute to regeneration defects. Results: By comparing gene expression between young (2 weeks old, n = 3) and aged (80 weeks old, n = 3) mice among four types of muscles, we identified that Tfr1 expression is declined in muscles of aged mice (~80% reduction, P < 0.005), so as to its protein level in SCs of aged mice. From in vivo and ex vivo experiments, Tfr1 deletion in SCs results in an irreversible depletion of SCs (~60% reduction, P < 0.005) and cell‐autonomous defect in SC proliferation and differentiation, leading to skeletal muscle regeneration impairment, followed by labile iron accumulation, lipogenesis, and decreased Gpx4 and Nrf2 protein levels leading to reactive oxygen species scavenger defects. These abnormal phenomena including iron accumulation, activation of unsaturated fatty acid biosynthesis, and lipid peroxidation are orchestrated with the occurrence of ferroptosis in skeletal muscle. Ferroptosis further exacerbates SC proliferation and skeletal muscle regeneration. Ferrostatin‐1, a ferroptosis inhibitor, could not rescue ferroptosis. However, intramuscular administration of lentivirus‐expressing Tfr1 could partially reduce labile iron accumulation, decrease lipogenesis, and promote skeletal muscle regeneration. Most importantly, declined Tfr1 but increased Slc39a14 protein level on cellular membrane contributes to labile iron accumulation in skeletal muscle of aged rodents (~80 weeks old), leading to activation of ferroptosis in aged skeletal muscle. This is inhibited by ferrostatin‐1 to improve running time ( P = 0.0257) and distance ( P = 0.0248). Conclusions: Satellite cell‐specific deletion of Tfr1 impairs skeletal muscle regeneration with activation of ferroptosis. This phenomenon is recapitulated in skeletal muscle of aged rodents and human sarcopenia. Our study provides mechanistic information for developing novel therapeutic strategies against muscular ageing and diseases.