OsBBX11 on qSTS4 links to salt tolerance at the seeding stage in Oryza sativa L. ssp. Japonica.

Rice has been reported to be highly sensitive to salt stress at the seedling stage. However, the lack of target genes that can be used for improving salt tolerance has resulted in several saline soils unsuitable for cultivation and planting. To characterize new salt-tolerant genes, we used 1,002 F2:3 populations derived from Teng-Xi144 and Long-Dao19 crosses as the phenotypic source to systematically characterize seedlings' survival days and ion concentration under salt stress. Utilizing QTL-seq resequencing technology and a high-density linkage map based on 4,326 SNP markers, we identified qSTS4 as a major QTL influencing seedling salt tolerance, which accounted for 33.14% of the phenotypic variation. Through functional annotation, variation detection and qRT-PCR analysis of genes within 46.9 Kb of qSTS4, it was revealed that there was one SNP in the promoter region of OsBBX11, which resulted in a significant response difference between the two parents to salt stress. Transgenic plants using knockout-based technology and demonstrated that Na+ and K+ in the roots of the functional-loss-type OsBBX11 were translocated largely to the leaves under 120 mmol/L NaCl compared with the wild-type, causing osbbx11 leaves to die after 12 days of salt stress due to an imbalance in osmotic pressure. In conclusion, this study identified OsBBX11 as a salt-tolerance gene, and one SNPs in the OsBBX11 promoter region can be used to identify its interacting transcription factors. This provides a theoretical basis for finding the molecular mechanism of OsBBX11 upstream and downstream regulation of salt tolerance and molecular design breeding in the future.

HuR Affects the Radiosensitivity of Esophageal Cancer by Regulating the EMT-Related Protein Snail.

Purpose: We previously found that Hu antigen R (HuR) can regulate the proliferation and metastasis of esophageal cancer cells. This study aims to explore the effects of HuR on the radiosensitivity of esophageal cancer. Materials and Method: Analyses of CCK-8, colony formation assay, Western blot, immunofluorescence, flow cytometry, reactive oxygen species (ROS), and mitochondrial membrane potential were conducted to characterize the esophageal cancer cells. Nude mouse models were used to detect the effects of HuR in a combination of X-ray treatment on the subcutaneous xenografts of esophageal cancer. In addition, a luciferase assay was used to detect the direct interaction of HuR with Snail mRNA 3'-UTR. Results: The down-regulation of HuR combined with X-ray can significantly inhibit the proliferation and colony formation of esophageal cancer cells. Flow cytometry data showed that the down-regulation of HuR could induce a G1 phase cell cycle block in esophageal cancer cells, and aggravate X-ray-induced apoptosis, indicated by the increases of apoptosis-related proteins Bax, caspase-3 and caspase-9. Moreover, the down-regulation of HuR could significantly impair the mitochondrial membrane potential and increase the ROS production and DNA double-strand break marker γH2AX expression in esophageal cancer cells that were exposed to X-rays. In vivo data showed that the down-regulation of HuR combined with radiation significantly decreased the growth of subcutaneous xenograft tumors. Furthermore, HuR could interact with Snail. Up-regulation of Snail can reverse the EMT inhibitory effects caused by HuR down-regulation, and attenuate the tumor-inhibiting and radiosensitizing effects caused by HuR down-regulation. Conclusion: In summary, our data demonstrate that HuR effectively regulates the radiosensitivity of esophageal cancer, which may be achieved by stabilizing Snail. Thus, HuR/Snail axis is a potentially therapeutic target for the treatment of esophageal cancer.

IFI35 is involved in the regulation of the radiosensitivity of colorectal cancer cells.

BACKGROUND: Interferon regulatory factor-1 (IRF1) affects the proliferation of colorectal cancer (CRC). Recombinant interferon inducible protein 35 (IFI35) participates in immune regulation and cell proliferation. The aim of the study was to examine whether IRF1 affects the radiation sensitivity of CRC by regulating IFI35. METHODS: CCL244 and SW480 cells were divided into five groups: blank control, IFI35 upregulation, IFI35 upregulation control, IFI35 downregulation, and IFI35 downregulation control. All groups were treated with X-rays (6 Gy). IFI35 activation by IRF1 was detected by luciferase reporter assay. The GEPIA database was used to examine IRF1 and IFI35 in CRC. The cells were characterized using CCK-8, EdU, cell cycle, clone formation, flow cytometry, reactive oxygen species (ROS), and mitochondrial membrane potential. Nude mouse animal models were used to detect the effect of IFI35 on CRC. RESULTS: IRF1 can bind to the IFI35 promoter and promote the expression of IFI35. The expression consistency of IRF1 and IFI35 in CRC, according to GEPIA (R = 0.68, p < 0.0001). After irradiation, the upregulation of IFI35 inhibited cell proliferation and colony formation and promoted apoptosis and ROS, while IFI35 downregulation promoted proliferation and colony formation and reduced apoptosis, ROS, and mitochondrial membrane potential were also reduced. The in vivo experiments supported the in vitro ones, with smaller tumors and fewer liver metastases with IFI35 upregulation. CONCLUSIONS: IRF1 can promote IFI35 expression in CRC cells. IFI35 is involved in the regulation of radiosensitivity of CRC cells and might be a target for CRC radiosensitization.

Colonic mucinous adenocarcinoma causing intussusception and distant metastasis: A case report.

RATIONALE: Cases of intussusception caused by mucinous carcinoma have been rarely reported, and those caused by colonic mucinous adenocarcinoma (MAC) with distant metastasis were even fewer. PATIENT CONCERNS: A 60-year-old woman who complained of severe pain around the navel with nausea and vomiting for a week was admitted on November 28, 2017. There were multiple watery stools and abdominal pain was worsened over the prior week. DIAGNOSIS: She was diagnosed by abdominal computed tomography, current medical history, and abdominal signs. Her initial diagnosis was acute abdomen, intussusceptions, and intestinal obstruction. The final diagnosis was MAC, which was based on postoperative pathology. INTERVENTIONS: The patient received emergency laparotomy, followed by 5 courses of chemotherapy with oxaliplatin plus capecitabine, and then 6 courses with 5-fluorouracil + oxaliplatin + calcium leucovorin. OUTCOMES: The patient was in good nutritional condition, and no obvious tumor recurrence or metastasis was found until July 9, 2018. LESSONS: Even though the prognosis of colonic MAC is poor, being able to receive timely surgical treatment, good nutritional status and reasonable postoperative chemotherapy are the key factors to prolonging patient's survival.

[MicroRNA-146a polymorphism and susceptibility to gastrointestinal cancer: a meta-analysis].

OBJECTIVE: To investigate the association between microRNA (miR)-146a gene polymorphisms and susceptibility to gastrointestinal cancer. METHODS: PubMed, Medline and Ovid full text databases, China Journal Full-text Database (CNKI), Articles Database and Chinese Biomedical Literature Database were researched to retrieved literatures about the association between miR-146a gene polymorphism and susceptibility to gastrointestinal cancer published from July 2010 to March 2014. Modified Jadad quality score was used to evaluate the quality of the literatures and Stata 11.0 software was used to analyze and calculate OR value of the following 5 different genotypes: allele (G vs. C), the dominant genetic model (GC+GG vs. CC), a recessive genetic model (GG vs. GC+CC) and homozygote (GG vs. CC) and heterozygote (GC vs. CC) to assess the association. RESULTS: A total of 16 studies were enrolled, including 7090 cancer patients and 9928 healthy controls. Meta-analysis showed that people with G allele was more susceptible to gastrointestinal cancer than those with C(gastric cancer: OR=1.1,95% CI:1.04-1.17, P=0.001, colorectal cancer: OR=1.09,95% CI:1.01-1.18, P=0.020); dominant model (GC+GG) was more susceptible to gastric cancer than CC (OR=1.12, 95% CI:1.02-1.22, P=0.016); recessive genetic model GG was more susceptible to gastrointestinal cancer than CC+GC (gastric cancer: OR=1.16, 95% CI:1.05-1.27, P=0.004, colorectal cancer: OR=1.13, 95%CI:1.00-1.28, P=0.047); GG homozygote was more susceptible to gastrointestinal cancer than CC (gastric cancer: OR=1.20, 95% CI:1.06-1.35, P=0.003, colorectal cancer: OR=1.19, 95% CI:1.01-1.41, P=0.042). Dominant genetic model GC+GG and CC in colorectal cancer as well as heterozygous GC and CC in gastrointestinal cancer were not significantly different(P>0.05). CONCLUSION: miR-146a cancer susceptibility gene polymorphism is closely associated with gastrointestinal cancers.