New insights into mechanisms and interventions of locoregional therapies for hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is responsible for a significant number of cancer-related deaths worldwide and its incidence is increasing. Locoregional treatments, which are precision procedures guided by imaging to specifically target liver tumors, play a critical role in the management of a substantial portion of HCC cases. These therapies have become an essential element of the HCC treatment landscape, with transarterial chemoembolization (TACE) being the treatment of choice for patients with intermediate to advanced stages of the disease. Other locoregional therapies, like radiofrequency ablation, are highly effective for small, early-stage HCC. Nevertheless, the advent of targeted immunotherapy has challenged these established treatments. Tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs) have shown remarkable efficacy in clinical settings. However, their specific uses and the development of resistance in subsequent treatments have led clinicians to reevaluate the future direction of HCC therapy. This review concentrates on the distinct features of both systemic and novel locoregional therapies. We investigate their effects on the tumor microenvironment at the molecular level and discuss how targeted immunotherapy can be effectively integrated with locoregional therapies. We also examine research findings from retrospective studies and randomized controlled trials on various combined treatment regimens, assessing their validity to determine the future evolution of locoregional therapies within the framework of personalized, comprehensive treatment.

FSTL3 promotes tumor immune evasion and attenuates response to anti-PD1 therapy by stabilizing c-Myc in colorectal cancer.

Programmed cell death 1 ligand 1 (PDL1)/programmed cell death 1 (PD1) blockade immunotherapy provides a prospective strategy for the treatment of colorectal cancer (CRC), but various constraints on the effectiveness of the treatment are still remaining. As reported in previous studies, follistatin-like 3 (FSTL3) could mediate inflammatory response in macrophages by induction lipid accumulation. Herein, we revealed that FSTL3 were overexpressed in malignant cells in the CRC microenvironment, notably, the expression level of FSTL3 was related to tumor immune evasion and the clinical efficacy of anti-PD1 therapy. Further studies determined that hypoxic tumor microenvironment induced the FSTL3 expression via HIF1α in CRC cells, FSTL3 could bind to the transcription factor c-Myc (354-406 amino acids) to suppress the latter's ubiquitination and increase its stability, thereby to up-regulated the expression of PDL1 and indoleamine 2,3-dioxygenase 1 (IDO1). The results in the immunocompetent tumor models verified that FSLT3 knockout in tumor cells increased the proportion of CD8+ T cells in the tumor microenvironment, reduced the proportion of regulatory T cells (CD25+ Foxp3+) and exhausted T cells (PD1+ CD8+), and synergistically improved the anti-PD1 therapy efficacy. To sum up, FSTL3 enhanced c-Myc-mediated transcriptional regulation to promote immune evasion and attenuates response to anti-PD1 therapy in CRC, suggesting the potential of FSTL3 as a biomarker of immunotherapeutic efficacy as well as a novel immunotherapeutic target in CRC.

The Influence of Preoperative Waiting Time on Anxiety and Pain Levels in Outpatient Surgery for Breast Diseases.

OBJECTIVE: This study aims to examine the effects of different preoperative waiting times on anxiety and pain levels in patients undergoing outpatient surgery for breast diseases, providing insights for clinical interventions during the perioperative phase. METHODS: Patients who underwent outpatient surgery at a hospital breast center in Ningbo between January 2021 and December 2021 were selected. Their anxiety levels at the time when they entered the preoperative preparation room and when they ended the postoperative waiting period for the rapid frozen section procedure were assessed using the State Anxiety Inventory (S-AI) questionnaire, and their pain levels at the end of the postoperative waiting period were assessed using the short-form McGill Pain Questionnaire. The patients enrolled were divided into 3 groups according to the preoperative waiting time: <2 hours (T1 group), 2 to 4 hours (T2 group), and >4 hours (T3 group); there were 150 patients in each group, and the anxiety and pain levels were compared between the groups. RESULTS: At the time of entering the preoperative preparation room, patients' S-AI score T1 = T2 ( P > 0.05), both T1 and T2 < T3 ( P < 0.05); however, at the time of the postoperative waiting period, patients' S-AI score was T1 < T2 < T3 ( P < 0.05), and the postoperative waiting period patients' short-form McGill Pain Questionnaire scores were T1 = T2 < T3 ( P < 0.05). CONCLUSIONS: The perioperative anxiety and pain levels of patients undergoing outpatient breast surgery increased with the prolongation of preoperative waiting time; 4 hours was the critical time point for change, after which the anxiety and pain levels of patients increased significantly.

Identification of candidate miRNA biomarkers correlated with the prognosis of cell carcinoma and endocervical adenocarcinoma via integrated bioinformatics analysis.

OBJECTIVES: This study was designed to explore MicroRNAs (miRNAs) associated with the prognosis of cell carcinoma and endocervical adenocarcinoma (CESC) to search for biomarkers of CESC and provide guidelines for the clinical treatment. METHODS: mRNAs of CESC patients were downloaded from The Cancer Genome Atlas (TCGA), and miRNA expression and clinical data of the patients were preprocessed. Key miRNAs associated with the prognosis of cervical cancer were identified by weighted gene co-expression network (WGCNA). The corresponding target genes were intersected with differentially expressed genes (DEGs) acquired from variation analysis, and the pathways and functional enrichment of genes were analyzed. Key genes were screened by Kaplan-Meier (K-M) survival analysis. Risk models were constructed using Cox proportional hazard regression model and the Least Absolute Shrinkage and Selection Operator (LASSO) method, and the predictive value of the models was evaluated by time-associated receiver operating characteristic (ROC) curves. Finally, independent prognostic factors were identified by COX analysis. RESULTS: The hsa-miR-3150b-3p associated with the prognosis of CESC was identified by WGCNA. A total of 136 target genes were differentially expressed in CESC tissue and were associated with biological processes such as phylogeny, multicellular organism development and cell development. CBX7, ENPEP, FAIM2, IGF1, NUP62CL and TSC22D3 were associated with the prognosis of CESC, and a prognostic prediction model was constructed using these six genes, which had a good predictive value for the prognosis of cervical cancer within 1, 3 and 5 years (AUC: 0.784, 0.680 and 0.683, respectively). Among them, ENPEP (hazard ratio = 1.3996, 95% confidence interval: 1.0552-1.8565) was identified as an independent prognostic factor. CONCLUSIONS: In this study, a highly accurate prognostic model consisting of six gene signatures was developed to predict the prognosis of patients with cervical cancer, which provides a reference for developing individualized treatment plans for patients.

Antitumour effects of apatinib in progressive, metastatic differentiated thyroid cancer (DTC).

PURPOSE: Management of progressive, metastatic radioactive iodine refractory differentiated thyroid cancer (RAIR-DTC) has been a great challenge due to its poor prognosis and limited treatment options. Recently, apatinib, an orally anti-angiogenic tyrosine kinase inhibitor (TKI) is reported to be useful for treatment of progressive RAIR-DIC. The aim of this study was to evaluate the antitumour effect of apatinib and the combination therapy with radioactive iodine (RAI) in patients with progressive metastatic DTC. METHODS: Five patients (all female, mean age 62 ± 8 years, ranged from 51 to 69 years) with distant metastatic DTC (dmDTC) after total thyroidectomy (TTE) and neck lymph node dissection were treated with apatinib at a dose 500 mg per day after 18F-Fluorodeoxyglucose (18F-FDG) PET/CT. The effects of apatinib on DTC were evaluated at 4 ± 1 months after treatment with apatinib. RAI therapy was then initiated. The response to apatinib and the combination therapy with RAI treatment was evaluated by Response Evaluation Criteria in Solid Tumours (RECIST, version 1.1) and metabolic activity using serum thyroglobulin (Tg) and 18F-FDG PET/CT. RESULTS: Positive 18F-FDG PET/CT results were found in all patients before apatinib therapy. The immunohistochemical analysis of primary tumour tissues showed high expression of vascular endothelial growth factor receptor-2 (VEGFR-2). Four patients with follicular thyroid carcinoma (FTC) showed partial response (PR) with significant decrease in tumour size and maximum standardized uptake value (SUVmax) after 4 ± 1 month's treatment with apatinib. Further significant reduction of tumour size and SUVmax were observed in three patients after combination therapy with apatinib and RAI. Only one patient with both FTC and papillary thyroid cancer (PTC) demonstrated progressive disease (PD) after treatment with apatinib alone, however, a decrease in tumour size and SUVmax as well as serum Tg levels was achieved after the combination with RAI therapy and apatinib. CONCLUSIONS: Apatinib had significant antitumour effects on progressive distant metastatic DTC. Moreover, beneficial synergistic and complementary effects were shown when apatinib combined with RAI therapy. CLINICAL TRIAL REGISTRATION: NCT04180007, Registered November 26, 2019.

Potential molecular mechanisms and clinical progress in liver metastasis of breast cancer.

Breast cancer is the most common malignant tumor in women and the leading cause of cancer death in women. About 30% of breast cancer patients have metastasis every year, which greatly increases the mortality rate of breast cancer. The main target organs for metastasis are bone, brain, liver and lung. The breast cancer liver metastasis (BCLM) mechanism is not fully clarified. This is a complex process involving multiple factors, which is not only related to the microenvironment of the primary tumor and liver, but also regulated by a variety of signaling pathways. Clarifying these mechanisms is of great help to guide clinical treatment. With the in-depth study of BCLM, a variety of new treatment schemes such as targeted therapy and endocrine therapy provide new ideas for the cure of BCLM. In this review, we will summarize the molecular mechanism and treatment of BCLM.

Knockdown of nuclear receptor binding SET domain-containing protein 1 (NSD1) inhibits proliferation and facilitates apoptosis in paclitaxel-resistant breast cancer cells via inactivating the Wnt/ß-catenin signaling pathway.

The burden of breast cancer (BC) has exacerbated over decades. Paclitaxel resistance is responsible for increasing BC treatment burden. Nuclear receptor binding SET domain-containing protein 1 (NSD1) is positively correlated with a poor prognosis in patients with BC. This study investigates the function of NSD1 in paclitaxel-resistant (PR) BC cells. The high levels of NSD1 and Wnt10b in PR BC cell lines (MCF-7/PR) or MCF-7 parental cells were determined by RT-qPCR. Western blotting was conducted to measure the levels of NSD1 protein, apoptosis-associated proteins, Wnt10b protein, H3K36me2 protein, H3K27me3 protein, and signal pathway-associated proteins in MCF-7/PR cells or MCF-7 cells or in vivo subcutaneous xenografted tumor model, and the results demonstrated that NSD1 inhibited cell apoptosis and promoted cell proliferation and tumor growth via activating Wnt/ß-catenin pathway. Cell apoptosis and viability were estimated using cell counting kit-8 assays and flow cytometry. Positive correlation between NSD1 and Wnt10b was identified by chromatin immunoprecipitation assay. The distribution of ß-catenin was determined by immunofluorescence assays. We conclude that NSD1 knockdown inhibits the viability and promotes the apoptosis of paclitaxel-resistant BC cells by inactivating the NSD1/H3K27me3/Wnt10b/ß-catenin signaling pathway.

Tegaserod Maleate Inhibits Breast Cancer Progression and Enhances the Sensitivity of Immunotherapy.

BACKGROUND: Breast cancer (BC) is the most commonly diagnosed cancer in women worldwide. The challenge in managing this heterogeneous malignancy is that BC is highly aggressive and is always associated with chemical resistance, radiation resistance, hormone therapy resistance, and targeted therapy resistance. Therefore, there is an urgent need to find effective drugs to treat BC. METHODS: Based on the Selleck drug library approved by FDA, we screened 800 drugs for anti-BC cells and found that tegaserod maleate (TM), a 5-hydroxytryptamine 4-receptor (HTR4) partial agonist had the best anti-BC effect, which was further verified. The effects of different concentrations of TM on cell proliferation, invasion, and migration were evaluated in vitro using CCK8, plate cloning, transwell, and scratch assays. The UALCAN database, Kaplan-Meier Plotter database, Human Protein Atlas, and GEPIA2 were used to explore the correlation between HTR4 expression and BC patients' clinicopathological data as well as immune response. In vivo experiments demonstrated the effect of the TM and immunotherapy drug (anti-PD1/anti-TIGIT) combination on BC tumor growth in mice. RESULTS: TM significantly inhibited the proliferation, invasion, and migration of BC cells, and the higher the concentration, the better the inhibition effect. HTR4 was significantly downregulated in BC tissues compared to paracancerous tissues. The downregulation of HTR4 was correlated with clinicopathological data and positively correlated with BC prognosis. Interestingly, the GEPIA2 database suggested that there was a strong positive correlation between the expression of HTR4 and effector T cells, effector memory T cells, and exhausted T cells. In vitro experiments showed that TM, anti-PD1, and anti-TIGIT could all inhibit the growth and weight of BC tumors as compared with the control group. However, when anti-PD1 or anti-TIGIT was used simultaneously with TM, the inhibition of tumors significantly exceeded that in the control group. Moreover, the combination of anti-TIGIT and TM has the best inhibitory effect. CONCLUSION: TM inhibited the progression of breast cancer, and its combination with anti-TIGIT could effectively inhibit tumor growth and improve the sensitivity of immunotherapy in breast cancer.

Upregulation of ADAR Promotes Breast Cancer Progression and Serves as a Potential Therapeutic Target.

BACKGROUND: Breast cancer (BC) is the most common cause of cancer death worldwide, and its incidence is increasing every year. This study aims to investigate the expression characteristics of ADAR gene in breast cancer and to explore its role in the occurrence and development of BC and its possible mechanism. METHODS: TCGA portal was used to detect the expression of ADAR in cancer including BC, and its correlation with clinicopathological data as well as other genes was analyzed via UALCAN database. The TISCH database evaluated the expression of ADAR in different types of cell populations in BC at the single-cell level. The Kaplan-Meier plotter database was used to predict the correlation between ADAR expression and BC patient prognosis. The Human Protein Atlas was used to detect the expression of ADAR in tissues and location of ADAR mRNA in cells. Moreover, the relationships between immune response and ADAR expression in BC were assessed with the use of the TISIDB. Metascape and STRING were applied to predict ADAR with other protein interactions. Finally, the effect generated by ADAR expression on cell proliferating, invading, and migrating processes was assessed in vitro with knockdown and overexpression strategies. RESULTS: ADAR was significantly upregulated in BC tissues compared to paracancerous tissues. Single-cell RNA analysis showed that ADAR was specifically upregulated in cancer cell clusters and was also expressed in stromal and immune cell clusters. The upregulation of ADAR was positively correlated with clinicopathological stage and negatively correlated with BC prognosis. Experimental processes in vitro revealed ADAR knockdown hindered, proliferated, invaded, and migrated levels of BC cells, whereas over expression of ADAR played the opposite effect. ADAR protein, which may interact with OASL, STAT2, and IFIT3, was mainly located in the nucleoli in cells and primarily involved DNA modification and apoptotic signaling pathway. Immune factors may interact with ADAR in BC, and ADAR was found noticeably linked with immunosuppressor such as IL10, CD274, and IDO1. CONCLUSION: ADAR is significantly upregulated in breast cancer tissues, which may promote the progression of BC through the interaction of cancer cells, stromal cells, and immune cells. Targeting ADAR may offer new hope in treating breast cancer.

Advances of circular RNAs in thyroid cancer: An overview.

Circular RNA (circRNA) is a general term for a type of single-stranded RNAs, they are primarily generated via exon back-splice process in precursor mRNAs (pre-mRNAs). circRNAs refer to an emerging type of endogeneity-correlated closed molecules of RNA in a covalent manner. They mainly function as microRNA sponges, protein brackets, and regulatory element in transcription and splicing process. Recently, it has also starting been noticed that they serve as extraordinary models involved in polypeptides producing process. Although circRNAs have been extensively studied, their function in thyroid carcinoma is still lacking. Thus, we present the latest advances in circRNA research and summarize their fundamental rules of regulating process as well as the mechanism. More importantly, We mainly review the role and mechanism of circRNA in thyroid cancer, which provides an emerging perspective and theoretically supports the treatment of thyroid cancer.

Emerging Mechanisms and Treatment Progress on Liver Metastasis of Colorectal Cancer.

Colorectal cancer is currently the third largest malignant tumor in the world, with high new cases and high mortality. Metastasis is one of the most common causes of death of colorectal cancer, of which liver metastasis is the most fatal. Since the beginning of the Human Genome Project in 2001, people have gradually recognized the 3 billion base pairs that make up the human genome, of which only about 1.5% of the nucleic acid sequences are used for protein coding, including proto-oncogenes and tumor suppressor genes. A large number of differences in the expression of proto-oncogenes and tumor suppressor genes have also been found in the study of colorectal cancer, which proves that they are also actively involved in the progression of colorectal cancer and promote the occurrence of liver metastasis. Except for 1.5% of the coding sequence, the rest of the nucleic acid sequence does not encode any protein, which is called non-coding RNA. With the deepening of research, genome sequences without protein coding potential that were originally considered "junk sequences" may have important biological functions. Many years of studies have found that a large number of abnormal expression of ncRNA in colorectal cancer liver metastasis, indicating that ncRNA plays an important role in it. To explore the role and mechanism of these coding sequences and non-coding RNA in liver metastasis of colorectal cancer is very important for the early diagnosis and treatment of liver metastasis of colorectal cancer. This article reviews the coding genes and ncRNA that have been found in the study of liver metastasis of colorectal cancer in recent years, as well as the mechanisms that have been identified or are still under study, as well as the clinical treatment of liver metastasis of colorectal cancer.

Application of Animal Models in Cancer Research: Recent Progress and Future Prospects.

Animal models refers to the animal experimental objects and related materials that can simulate human body established in medical research. As the second-largest disease in terms of morbidity and mortality after cardiovascular disease, cancer has always been the focus of human attention all over the world, which makes it a research hotspot in the medical field. At the same time, more and more animal models have been constructed and used in cancer research. With the deepening of research, the construction methods of cancer animal models are becoming more and more diverse, including chemical induction, xenotransplantation, gene programming, and so on. In recent years, patient-derived xenotransplantation (PDX) model has become a research hotspot because it can retain the microenvironment of the primary tumor and the basic characteristics of cells. Animal models can be used not only to study the biochemical and physiological processes of the occurrence and development of cancer in objects but also for the screening of cancer drugs and the exploration of gene therapy. In this paper, several main tumor animal models and the application progress of animal models in tumor research are systematically reviewed. Finally, combined with the latest progress and development trend in this field, the future research of tumor animal model was prospected.

Circ-TFCP2L1 Promotes the Proliferation and Migration of Triple Negative Breast Cancer through Sponging miR-7 by Inhibiting PAK1.

CircRNAs are essential factors that have been verified to regulate various forms of carcinogenesis. However, the role of circRNAs in triple negative breast cancer (TNBC) tumourigenesis is not well clarified. In this study, we explored the circRNA expression profiles and possible modulation mechanism of circRNAs on triple negative breast cancer tumourigenesis. We used three pairs of triple negative breast cancer tissues and adjacent noncancerous tissues to perform a human circRNA microarray for screening of circRNA expression patterns in TNBC. The results showed that circ-TFCP2L1 was significantly up-regulated in TNBC tissues and cells, tending to have a shorter disease-free survival of TNBC patients. In vitro loss-of-function experiments showed that knockdown of circ-TFCP2L1 significantly suppressed the proliferation and migration of TNBC cells. Moreover, the results showed that the proliferation and migration capabilities and PAK1 expression in TNBC cells treated with si-circ-TFCP2L1 + miR-7 mimics were significantly suppressed compared with the normal group. Therefore, circ-TFCP2L1 was identified as a sponge of miR-7 functionally targeting PAK1 and further promoting the proliferation and migration of TNBC cells. Taken together, the results from our study reveal a novel regulatory mechanism and offer novel insight into the role of circ-TFCP2L1 in progression of triple negative breast cancer.

Star Circular RNAs In Human Cancer: Progress And Perspectives.

Circular RNAs (circRNAs) are a recently discovered subclass of non-coding RNAs (ncRNAs) characterized by a covalently closed loop structure created by reverse splicing. Because they do not have a 5' cap structure and a 3' poly A tail, circRNAs have higher stability, abundance and evolutionary conservation than linear RNA between species. These features produce various potential biological functions of circRNAs, such as miRNA sponges, RNA-binding proteins that form RNA protein complexes. In recent years, more and more studies have shown that circRNAs play a vital role in the occurrence and development of human diseases. At the same time, their enormous potential as a biomarker and therapeutic target is also evolving. The purpose of this review is to summarize existing cancer-associated circRNAs and to try to find circRNAs that are abnormally expressed in many cancers. Therefore, we reviewed previous circRNAs studies related to cancer and selected them by statistics. The eight circRNAs that have the highest frequency in different cancers or involve key pathways are called star circRNAs. Here, we review the classification, features, and functions of emerging star circRNAs, with particular attention to the role of circRNAs in various cancers.

Up-regulation of SPC25 promotes breast cancer.

In this study, expression of the SPC25 gene was characterized in breast cancer (BC), and its effects on BC development and progression, functions in BC cells, and potential underlying mechanisms were examined. Data from TCGAportal and FIREBROWSE indicated that SPC25 was upregulated in BC tissues compared to normal tissues, and CANCERTOOL indicated that higher SPC25 mRNA levels were associated with increased probability of recurrence and poorer survival in BC patients. BC patients with higher SPC25 expression displayed shorter distant metastasis-free survival, relapse-free survival, and overall survival. Colony formation and CCK-8 experiments confirmed that SPC25 promoted proliferation of BC cells. Single-cell analysis indicated that SPC25 is associated with cell cycle regulation, DNA damage and repair, and BC cell proliferation. SPC25 knockdown suppressed proliferation of BC cells. MiRNAs, circRNAs, RNA-binding proteins, transcription factors, and immune factors that might interact with SPC25 mRNA to promote BC were also identified. These findings suggest that SPC25 levels are higher in more malignant BC subtypes and are associated with poor prognosis in BC patients. In addition, DNA methyltransferase inhibitor and transcription factors inhibitor treatments targeting SPC25 might improve survival in BC patients.

CircRNA microarray profiling identifies a novel circulating biomarker for detection of gastric cancer.

CircRNA expression profiles for gastric cancer (GC) were screened using plasma samples from 10 GC patients with different TNM stages and 5 healthy individuals as controls. Results showed lower expression of circ-KIAA1244 in GC tissues, plasmas, and cells compare to normal controls. Further clinical data analysis demonstrated that a decreased expression of circ-KIAA1244 in plasmas was negatively correlated with TNM stage and lymphatic metastasis, and a shorter overall survival time of GC patients. Moreover, we found that circ-KIAA1244 could be detected in GC plasma exosomes and showed no obvious significance compared to the expression level in the corresponding plasmas. This study revealed a GC-tissues-derived circ-KIAA1244 could serve a novel circulating biomarker for detection of GC.

Circular RNAs as novel rising stars with huge potentials in development and disease.

Circular RNAs (circRNAs), which were discovered as a special class of endogenous non-coding RNAs, have recently shown huge capabilities as gene regulators in different species in a wide variety of organisms including viruses, plants, archaea and animals. These circRNAs mainly arise from exons or introns in different combinations by special selective splicing and are enriched in cytoplasm. Apart from that, circRNAs usually display patterns of cell-type, tissue-type and developmental-stage specific expression in eukaryotic transcriptome. These findings hint at the vital function of circRNAs in development and diseases. Herein, we summarize the current understanding of the molecular characteristics of circRNAs and discuss their proposed functions and mechanism-of-action in human diseases, animals as well as botanics.

Upregulation of circ_0066444 promotes the proliferation, invasion, and migration of gastric cancer cells.

BACKGROUND: Circular RNAs (circRNAs), which have closed-loop structure, are involved in the pathogenesis of human diseases including various types of carcinomas. The present study aimed to investigate the relationship between a new circular RNA named circ_0066444 and gastric cancer (GC) carcinogenesis. MATERIALS AND METHODS: The circ_0066444 levels in 106 paired gastric carcinoma tissues and related adjacent normal tissues were detected by real-time quantitative reverse-transcription polymerase chain reaction. The correlation between the expression of circ_0066444 and clinicopathological features was analyzed. The impact of circ_0066444 expression on cell proliferation, invasion, as well as migration was evaluated in vitro using knockdown expression strategies. Finally, a network of circ_0066444-targeted miRNA interactions and their corresponding mRNAs was constructed. RESULTS: circ_0066444 was found to be significantly upregulated in 106 GC tissues as compared with paired adjacent nontumorous tissues (P=0.025), showing a high positive correlation with lymphatic metastasis (P=0.023). Furthermore, in vitro assays of the GC cell lines BGC-823 and AGS demonstrated that knockdown of circ_0066444 reduced cell proliferation, invasion, and migration significantly. Prediction and annotation revealed circ_0066444 was able to sponge to 5 miRNAs and 15 corresponding target mRNAs. CONCLUSION: Our study indicated upregulation of circ_0066444 promotes gastric cell proliferation, invasion, and migration ability and might serve as a novel biomarker for GC.

ERCC1 rs3212986 A/C polymorphism is not associated with chemotherapy treatment outcomes in gastric cancer patients: evidence from 11 publications in Chinese populations.

BACKGROUND: A number of studies have investigated the roles of excision repair cross-complementation group 1 (ERCC1) gene rs3212986 polymorphisms as potential biomarkers in gastric cancer (GC). However, the results were inconsistent. Here, we performed a meta-analysis to explore ERCC1 rs3212986 polymorphisms in the chemotherapy response and clinical outcome of GC. METHODS: PubMed, Embase, and Web of Science were searched up to July 28, 2017, for studies on the association between ERCC1 rs3212986 A/C polymorphisms and response to chemotherapy as well as overall survival time of GC. A fixed-effect or random-effect model was used to calculate the pooled odds ratios (ORs) based on the results from the heterogeneity tests. RESULTS: The result revealed that there was no significant association between the ERCC1 rs3212986 A/C polymorphism and response to chemotherapy in GC under comparison models (AA + CA versus CC, OR 0.95, P=0.80, AA versus CA, OR 0.85, P=0.55, AA versus CC, OR 0.74, P=0.47). Further identification suggested that ERCC1 rs3212986 A/C polymorphisms were not linked with the overall survival of GC (AA + CA versus CC, OR 1.09, P=0.52, AA versus CA, OR 1.05, P=0.85, AA versus CC, OR 1.43, P=0.23). CONCLUSION: Our meta-analysis indicated that the ERCC1 rs3212986 A/C polymorphism was not associated with response to chemotherapy or overall survival time in GC. Well-designed studies with larger sample sizes and more ethnic groups should be performed to further validate our results.