Precision radiotherapy, which accurately delivers the dose on a tumor and confers little or no irradiation to the surrounding normal tissue and organs, results in maximum tumor control and decreases the toxicity to the utmost extent. Proton beam therapy (PBT) provides superior dose distributions and has a dosimetric advantage over photon beam therapy. Initially, the clinical practice and study of proton beam therapy focused on ocular tumor, skull base, paraspinal tumors (chondrosarcoma and chordoma), and unresectable sarcomas, which responded poorly when treated with photon radiotherapy. Then, it is widely regarded as an ideal mode for reirradiation and pediatrics due to reducing unwanted side effects by lessening the dose to normal tissue. During the past decade, the application of PBT has been rapidly increasing worldwide and gradually expanding for the treatment of various malignancies. However, to date, the role of PBT in clinical settings is still controversial, and there are considerable challenges in its application. We systematically review the latest advances of PBT and the challenges for patient treatment in the era of precision medicine.

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Background Gastric cancer (GC), as one of the most common malignancies across the globe, is the fourth leading cause of cancer-related deaths. Though a large body of research has been conducted to develop the therapeutic methods of GC, the survival rate of advanced patients is still poor. We aimed to dig into the potential regulatory mechanism of GC progression. Methods Bioinformatics tools and fundamental assays were performed at first to confirm the candidate genes in our study. The functional assays and mechanism experiments were conducted to verify the regulatory mechanisms of the genes underlying GC progression. Results Long non-coding RNA (lncRNA) SND1 intronic transcript 1 (SND1-IT1) is highly expressed in exosomes secreted by GC cells. SND1-IT1 was verified to bind to microRNA-1245b-5p (miR-1245b-5p) through competitive adsorption to promote ubiquitin specific protease 3 (USP3) messenger RNA (mRNA) expression. SND1-IT1 was validated to recruit DEAD-box helicase 54 (DDX54) to promote USP3 mRNA stability. SND1-IT1 induces malignant transformation of GES-1 cells through USP3. USP3 mediates the deubiquitination of snail family transcriptional repressor 1 (SNAIL1). Conclusions Exosome-mediated lncRNA SND1-IT1 from GC cells enhances malignant transformation of GES-1 cells via up-regulating SNAIL1. Graphical Abstract

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Celecoxib, a specific cyclooxygenase-2 (COX-2) inhibitor, is a traditional nonsteroidal antipyretic analgesic and anti-inflammatory drug commonly used in clinic, which has inhibitory effect on colorectal cancer, gastric cancer, and other malignant tumors. This study showed that Celecoxib could significantly reverse the invasion and metastasis of gastric cancer and improved the pathological changes due to GC. We collected the clinical specimens to analyze the correlation between the expression of Lnc_AC006548.28, miR-223, and LAMC2. In the mouse model, Celecoxib can slowdown the growth of GC tumor and the occurrence of this effect may depend on Lnc_AC006548.28-miR-223-LAMC2 pathway, in vitro transfection, RT-PCR, western blot, CCK8, small chamber assay, flow cytometry, and immunohistochemistry to retest the protective effect of celecoxib. Our results showed that Celecoxib could reverse invasion and metastasis of gastric cancer through Lnc_AC006548.28-miR-223-LAMC2 pathway.