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Simple Summary: Gastric cancer (GC) is the world's third greatest cause of cancer-related death. Since the underlying pathogenic mechanisms are still unclear and only a limited number of specialized drugs have been developed, treating GC patients in clinical practice remains challenging. We observed that ATF4 was markedly upregulated in gastric cancer (GC) using immunohistochemistry and Western blotting assays in 80 paraffin-embedded GC samples and 4 fresh samples and para-cancerous tissues. The mechanism of ATF4 as a transcription factor in gastric cancer remains unclear. ATF4 knockdown using lentiviral vectors strongly inhibited the proliferation and invasion of GC cells. ATF4 upregulation using lentiviral vectors promoted the proliferation and invasion of GC cells. We observed that transcription factor ATF4 is bound to the promoter region of SHH to activate the Sonic Hedgehog pathway. Mechanistically, rescue assays showed that ATF4 regulated gastric cancer cells' proliferation and invasive ability through SHH. Activating transcription factor 4 (ATF4) is a DNA-binding protein widely generated in mammals, which has two biological characteristics that bind the cAMP response element (CRE). The mechanism of ATF4 as a transcription factor in gastric cancer affecting the Hedgehog pathway remains unclear. Here, we observed that ATF4 was markedly upregulated in gastric cancer (GC) using immunohistochemistry and Western blotting assays in 80 paraffin-embedded GC samples and 4 fresh samples and para-cancerous tissues. ATF4 knockdown using lentiviral vectors strongly inhibited the proliferation and invasion of GC cells. ATF4 upregulation using lentiviral vectors promoted the proliferation and invasion of GC cells. We predicted that the transcription factor ATF4 is bound to the SHH promoter via the JASPA database. Transcription factor ATF4 is bound to the promoter region of SHH to activate the Sonic Hedgehog pathway. Mechanistically, rescue assays showed that ATF4 regulated gastric cancer cells' proliferation and invasive ability through SHH. Similarly, ATF4 enhanced the tumor formation of GC cells in a xenograft model. [ABSTRACT FROM AUTHOR]

Simple Summary: The gut microbiome can regulate the long non-coding RNAs (lncRNAs) expression, which subsequently impacts the host transcriptome to change the expression of downstream target molecules, ultimately resulting in the development and progression of colorectal cancer (CRC). We focused on the important role of the microbiome in CRC and their effects on CRC-related lncRNAs. The aim of our study was to illustrate the mechanisms by which the gut microbiome mediated the occurrence and progression of CRC through the regulation of lncRNAs, because the regulatory role of the gut microbiome-induced lncRNAs in CRC has great potential and may serve as the foundation for future clinical CRC treatment, such as probiotic supplements and lncRNAs intervention. Although an imbalanced gut microbiome is closely associated with colorectal cancer (CRC), how the gut microbiome affects CRC is not known. Long non-coding RNAs (lncRNAs) can affect important cellular functions such as cell division, proliferation, and apoptosis. The abnormal expression of lncRNAs can promote CRC cell growth, proliferation, and metastasis, mediating the effects of the gut microbiome on CRC. Generally, the gut microbiome regulates the lncRNAs expression, which subsequently impacts the host transcriptome to change the expression of downstream target molecules, ultimately resulting in the development and progression of CRC. We focused on the important role of the microbiome in CRC and their effects on CRC-related lncRNAs. We also reviewed the impact of the two main pathogenic bacteria, Fusobacterium nucleatum and enterotoxigenic Bacteroides fragilis, and metabolites of the gut microbiome, butyrate, and lipopolysaccharide, on lncRNAs. Finally, available therapies that target the gut microbiome and lncRNAs to prevent and treat CRC were proposed. [ABSTRACT FROM AUTHOR]

Simple Summary: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with a high degree of immune tolerance. Galectins induce induction of immune evasion behavior in tumor cells. Galectins each play a role in promoting PDAC progression during PDAC immune evasion by coordinating the function and number of immune cells, especially galectin-1. In this paper. we review the involvement of galectins in the construction of PDAC privileged zones by regulating relevant immune cells, establishing fibrotic barriers, and promoting cellular metabolism. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and is highly immune tolerant. Although there is immune cell infiltration in PDAC tissues, most of the immune cells do not function properly and, therefore, the prognosis of PDAC is very poor. Galectins are carbohydrate-binding proteins that are intimately involved in the proliferation and metastasis of tumor cells and, in particular, play a crucial role in the immune evasion of tumor cells. Galectins induce abnormal functions and reduce numbers of tumor-associated macrophages (TAM), natural killer cells (NK), T cells and B cells. It further promotes fibrosis of tissues surrounding PDAC, enhances local cellular metabolism, and ultimately constructs tumor immune privileged areas to induce immune evasion behavior of tumor cells. Here, we summarize the respective mechanisms of action played by different Galectins in the process of immune escape from PDAC, focusing on the mechanism of action of Galectin-1. Galectins cause imbalance between tumor immunity and anti-tumor immunity by coordinating the function and number of immune cells, which leads to the development and progression of PDAC. [ABSTRACT FROM AUTHOR]

Simple Summary: The intraoperative navigation techniques develop rapidly, we present an update on current use and research on indocyanine green enhanced fluorescence imaging (ICG-FI) guided lymphangiography in gastric oncological surgery. ICG serves as a promising tattooed agent for lymphangiography, its application was restricted by the false negative lymph nodes and loss of specificity in targeting tumor cells. Besides, we summarized the current approaches for gain in sensitivity and specificity of ICG-FI guided lymphangiography in gastric oncological surgery. The next direction for reinforced ICG-FI was quantification of ICG intensity and detection of ICG distribution pattern, combining with intraoperative biopsy method. Huge strides have been made in the navigation of gastric cancer surgery thanks to the improvement of intraoperative techniques. For now, the use of indocyanine green (ICG) enhanced fluorescence imaging has received promising results in detecting sentinel lymph nodes (SLNs) and tracing lymphatic drainages, which make it applicable for limited and precise lymphadenectomy. Nevertheless, issues of the lack of specificity and unpredictable false-negative lymph nodes were encountered in gastric oncologic surgery practice using ICG-enhanced fluorescence imaging (ICG-FI), which restrict its application. Here, we reviewed the current application of ICG-FI and assessed potential approaches to improving ICG-FI. [ABSTRACT FROM AUTHOR]