前言胃癌，作为一种来源于胃粘膜上皮细胞的恶性肿瘤，是全球癌症死亡的主要

Preface <br>Gastric cancer, as a malignant tumor derived from epithelial cells of the gastric mucosa, is one of the leading causes of cancer deaths in the world (1). Its incidence ranks fifth in the world, second only to lung cancer, breast cancer, colorectal cancer and prostate cancer. [1-2]. <br><br>With the advancement of science and technology and biotechnology, the level of early diagnosis of gastric cancer has improved, and a significant increase can be seen in the 5-year survival rate. <br><br>Nevertheless, the 5-year survival rate is only about 30% due to the easy recurrence and metastasis of advanced gastric cancer [3-4]. <br><br>Local recurrence and distant metastasis of tumors may be the most common causes of death (6). <br><br>The carcinogenesis and progression of gastric cancer involve environmental and genetic factors, and is a multi-step process (7-9). <br><br>The survival and prognosis of gastric cancer patients have so far been greatly improved by chemotherapy, radiotherapy, surgery, molecular targeted therapy and immunotherapy, but the underlying molecular mechanism is still unclear, and further research needs to be carried out (10). <br><br>This is, therefore, of great significance to study genes involved in metastasis, tumor progression and invasion, as well as to determine the molecular mechanism of the role of these genes in the treatment and prognosis of gastric cancer. <br><br>Efforts are currently being made to find molecular regulators of this particular invasion behavior. <br><br>One way is to look for actin regulatory proteins that may become targets for future anti-cancer treatments. In many cellular processes, the formin protein family coordinates the rearrangement of the actin cytoskeleton. <br>The remodeling of the actin cytoskeleton is crucial in cell migration, which is mediated by actin regulatory proteins, which are active in different cell locations. <br><br><br>Formins, as highly conserved actin nucleating proteins, are usually found in all eukaryotes. <br><br>Individual formins are usually inactive until activated or phosphorylated by Rho GTPases. <br><br>Rho GTPases have a variety of biochemical and functional properties in the formation of actin filaments, such as remodeling the cytoskeleton of different cell compartments, controlling the assembly of stress fibers, the formation of adhesion points, and the movement of cancer cells.<br><br>However, the role of formin protein in clinical tumor tissues has not received widespread attention. <br><br><br>Studies have found that the formin protein FMNL2, which is structurally similar to FHOD1 (formin homology 2 domain containing protein 1), is highly expressed in colon cancer tissues and is related to its metastasis [9]. <br><br>Despite the above findings [10-13], the lack of evaluation has generally not fully understood the clinical and pathological significance of FHOD1 in gastric cancer. <br><br>In this study, Cancer Genome Atlas (TCGA) data was used to analyze the expression of FHOD1 in GC. <br><br>The relationship between the overall survival rate of gastric cancer patients and the expression of FHOD1 was analyzed with the help of gastric cancer patient data obtained from the previous panomics experiment. <br><br><br>The role of FHOD1 in GC was explored through a series of experiments. This result provides important information for explaining the pathogenesis of GC and reveals that FHOD1 may be a potential new target for the treatment of gastric cancer. <br><br>Discussion <br><br>This study was carried out with its main purpose to study the biological role of FHOD1 in human gastric cancer cells and to clarify the role of FHOD1 in the development of gastric cancer. <br><br>Gastric cancer is usually a multifactorial process involving the degradation, spread, basement membrane, cell adhesion, angiogenesis, and movement of the extracellular matrix (21-25). <br><br>This is, therefore, crucial to identify new biomarkers for improving the clinical outcome of gastric cancer patients. <br>Formins are highly conserved actin nucleated proteins, which exist in all eukaryotes. <br>The activity of formins is regulated by Rho GTPases, a molecular switch that reshapes the cytoskeleton in different cell compartments. Rho GTPases can control the assembly of stress fibers, the formation of adhesion foci, and the movement pattern of cancer cells. <br>Maria Gardberg et al found that fhod1, a member of the formin family, is upregulated in squamous cell carcinoma EMT, and affects the morphological and functional characteristics of EMT: actin The ability of tissues, cells to migrate and degrade extracellular matrix<br><br>FHOD1 may mediate changes in the cytoskeleton and migration characteristics of cancer-related EMT in a variety of cancer types. <br>FHOD1 was found to be involved in migration or invasion earlier, and was upregulated in clinical tumor tissues of basal-like breast cancer [15]. In addition, FHOD1 is It has also been found to be expressed in oral squamous cell carcinoma and melanoma, and is also involved in migration/invasion in vitro [13,20]. <br><br>In this study, the screening of the TCGA database showed that the expression level of FHOD1 in GC tissues was significantly higher than that of adjacent non-tumor tissues. In addition, FHOD1 is moderately expressed in HGC27 and MKN45 cell lines.

Objective.<br>Stomach cancer, as a malignant tumor derived from the epithelat cells of the stomach mucous membrane, is one of the leading causes of cancer death (1) in the world, with the fifth highest incidence rate in the world, after lung, breast, colorectal and prostate cancers.<br><br>With the progress of science and technology and biotechnology, the early diagnosis level of stomach cancer has been improved, which can be seen in the five-year survival rate.<br><br>Nevertheless, the five-year survival rate is only about 30% due to the easy recurrence and metastasis of developing stage stomach cancer.<br><br>Local recurrence and distant metastasis of tumors may be the most common causes of death (6).<br><br>The cancer and progression of stomach cancer involves environmental and genetic factors and is a multi-step process (7-9).<br><br>The survival and prognostication of patients with stomach cancer has been greatly improved so far through chemotherapy, radiotherapy, surgery, molecular targeting therapy and immunotherapy, but their underlying molecular mechanisms are not yet known and further research is needed (10).<br><br>This is, therefore, important to study the molecular mechanisms involved in metastasis, tumor progress and invasion, and to determine the role of these genes in the treatment and prediction of gastric cancer prognosmation.<br><br>Efforts are currently being made to find molecular regulators for this particular intrusion.<br><br>One way to do this is to look for an action protein that could be a target for future anti-cancer treatments. In a variety of cellular processes, the formin protein family coordinates the rearracing of the tumor protein cytoskeletal skeleton.<br>The remodeling of the amyoglobin cytoskelete is important in cell migration, which is mediated by the myoglobin regulatory proteins, which are active at different cell locations.<br><br>Formins, as a highly conservative actoprotein nucleation protein, is usually found in all eosymical organisms.<br><br>Individualformins are usually inactive until activated or phosphate by Rho GTPases.<br><br>Rho GTPases has a variety of biotic and functional properties in the formation of myocardial protein filaments, such as remodeling the cytoskeletes of different cell chambers to control the assembly of stress fibers, the formation of adhesion points, and the movement of cancer cells.<br><br>However, the role of formin protein in clinical tumor tissue has not been widely concerned.<br><br>The study found that the formin protein FMNL2, similar to the structure of FHOD1 (formin homois 2 domain containing protein 1), was highly expressed in colon cancer tissue and was associated with its metastasis.<br><br>Despite the above findings, the molecular mechanism of the role of FHOD1 in gastric cancer is not fully understood in general.<br><br>In this study, Cancer Genome Atlas (TCGA) data was used to analyze the expression of FHOD1 in GC.<br><br>The relationship between the overall survival rate of gastric cancer patients and the expression of FHOD1 was analyzed by using data from the previous panomics experiment.<br><br>The role of FHOD1 in GC has been explored through a series of experiments. The results provide important information to explain the pathogenesis of GC and reveal that FHOD1 may be a potential new target for the treatment of stomach cancer.<br><br>Discuss.<br><br>The main purpose of this study was to study the biological role of FHOD1 in human stomach cancer cells and to clarify the role of FHOD1 in the development of stomach cancer.<br><br>Gastric cancer is usually a multi-factor process involving the degradation, transmission, substrate membrane, cell adhesion, angiogenesy and movement of extracellular substrates (21-25).<br><br>This is, therefore, critical to identify new biomarkers for improving clinical outcomes in patients with stomach cancer.<br>Formins is a highly conservative fibrin nucleated protein found in all eosymical organisms.<br>The activity of formins is regulated by Rho GTPases, a molecular switch that reshapes the cytostebrae within different cell spacings. Rho GTPases controls the assembly of stress fibers, the formation of adhesive stoves, and the movement patterns of cancer cells.<br>Maria Gardberg et al found that fhod1, a member of the formin family, was raised in squamous cell carcinoma EMT and affected the morphological and functional characteristics of EMT: the ability of the amyorotein tissue, cell migration, and degradation of the extracellular substation.<br><br>FHOD1 may mediate changes and migration characteristics of cytostebrae in various cancer-related EMTs.<br>FHOD1 was earlier found to be involved in migration or invasion, and was raised in the clinical tumor tissue of substrate-like breast cancer, in addition, FHOD1 was also found to be expressed in oral squamous cell carcinoma and melanoma, as well as in in-body involvement in migration/invasion.<br><br>In this study, screening of the TCGA database showed a significant increase in the level of expression of FHOD1 in GC tissue compared to neighboring non-tumor tissue. In addition, FHOD1 is moderately expressed in HGC27 and MKN45 cell line.

preface<br>Gastric cancer, as a malignant tumor originates from gastric epithelial cells, is one of the main causes of cancer death worldwide (1), the incidence rate is fifth in the world, second only to lung cancer, breast cancer, colorectal cancer and prostate cancer [1-2].<br>With the progress of science and technology and biotechnology, the early diagnosis of gastric cancer has been improved, which can be seen in the 5-year survival rate.<br>However, the 5-year survival rate is only about 30%, which is due to the recurrence and metastasis of advanced gastric cancer.<br>Local recurrence and distant metastasis may be the most common causes of death (6).<br>The carcinogenesis and progression of gastric cancer involves environmental and genetic factors, which is a multi-step process (7-9).<br>The survival and prognosis of patients with gastric cancer have been greatly improved by chemotherapy, radiotherapy, surgery, molecular targeted therapy and immunotherapy, but the underlying molecular mechanism is still unclear, and further research needs to be carried out (10).<br>Therefore, it is of great significance to study the genes involved in metastasis, tumor progression and invasion, as well as to determine the molecular mechanism of the role of these genes in the treatment and prognosis of gastric cancer.<br>Efforts are being made to find molecular regulators of this particular invasion.<br>One of the methods is to search for actin regulatory proteins which may be the target of future anticancer therapy. In a variety of cellular processes, the formin family coordinates actin cytoskeleton rearrangement.<br>Actin cytoskeleton remodeling is crucial in cell migration, which is mediated by actin regulatory proteins, which are active in different cell locations.<br>Formins, as a highly conserved actin nucleoprotein, is usually found in all eukaryotes.<br>Single formins are usually inactive until they are activated or phosphorylated by Rho GTPases.<br>Rho GTPases has a variety of biochemical and functional properties in the formation of actin filaments, such as remodeling the cytoskeleton of different intercellular compartments, controlling the assembly of stress fibers, the formation of adhesion points and the movement of cancer cells.<br>However, the role of formin in clinical tumor tissues has not been widely concerned.<br>It has been found that FMNL2, which is similar to FHOD1, is highly expressed in colon cancer tissues, which is related to its metastasis [9].<br>In spite of the above findings [10-13], there is a lack of evaluation for the clinicopathological significance of FHOD1 in gastric cancer, and the molecular mechanism of its role is not fully understood.<br>In this study, Cancer Genome Atlas (TCGA) data were used to analyze FHOD1 expression in GC.<br>The relationship between the overall survival rate and the expression of FHOD1 in gastric cancer patients was analyzed with the help of data from previous panomics experiments.<br>The role of FHOD1 in GC was discussed by a series of experiments. These results provide important information for the pathogenesis of GC and reveal that FHOD1 may be a potential new target for the treatment of gastric cancer.<br>discuss<br>The main purpose of this study is to study the biological role of FHOD1 in human gastric cancer cells, and to clarify the role of FHOD1 in the development of gastric cancer.<br>Gastric cancer is usually a multifactorial process involving extracellular matrix degradation, transmission, basement membrane, cell adhesion, angiogenesis and motility (21-25).<br>It is, therefore, crucial to identify new biomarkers for improving clinical outcomes in patients with gastric cancer.<br>Formins is a highly conserved actin nucleoprotein, which exists in all eukaryotes.<br>The activity of formins is regulated by Rho GTPases, a molecular switch that reshapes cytoskeleton in different intercellular spaces. Rho GTPases can control the assembly of stress fibers, the formation of adhesion foci and the movement pattern of cancer cells<br>Maria gardberg et al found that FHOD1, a member of the formin family, was up-regulated in EMT of squamous cell carcinoma and affected the morphological and functional characteristics of EMT: actin tissue, cell migration and extracellular matrix degradation ability<br>FHOD1 may mediate cytoskeleton alteration and migration in cancer associated EMT of various cancer types<br>FHOD1 was found to be involved in migration or invasion earlier, and was up-regulated in clinical tumor tissues of basal like breast cancer [15]. In addition, FHOD1 expression was also found in oral squamous cell carcinoma and melanoma, and also involved in migration / invasion in vitro [13,20].<br>In this study, screening of TCGA database showed that the expression level of FHOD1 in GC tissues was significantly higher than that in adjacent non tumor tissues. In addition, FHOD1 was moderately expressed in hgc27 and MKN45 cell lines.<br>