Decreased SLC16A13 Expression Level Can Increase Apoptosis in KATO2 Cell Line, A Promising Biomarker.

OBJECTIVE: Gastric cancer is a prevalent cancer type worldwide, and significant research efforts are focused on finding effective treatments. Recent studies have highlighted the importance of plasma membrane carriers, particularly solute carriers, in cancer progression. The SLC16A family, notably the SLC16A13 gene, plays a critical role in cancer development and tumor growth. This study aims to explore the impact of reducing SLC16A13 expression in gastric cancer cells on their survival, proliferation, and metastatic potential. METHODS: Gastric cancer cells (KATO2) were cultured in RPMI medium supplemented with 10% fetal bovine serum. The cells were then transfected with SLC16A13 si-RNA to lower gene expression. The effects of this si-RNA on cell death and apoptosis were assessed using MTT and flow cytometry assays. Cell migration capabilities were evaluated using the scratch test. Western blot and Real-Time PCR were employed to measure SLC16A13 expression levels and protein detection. Additionally, RT-PCR was used to analyze changes in genes related to apoptosis and cell migration. RESULTS: The reduction of SLC16A13 expression following si-RNA transfection significantly increased apoptosis and cell death in the KATO2 cell line after 72 hours (P < 0.0001). Furthermore, the study revealed that decreased SLC16A13 expression did not impact cancer cell migration. Cell viability, assessed by MTT assay, showed a significant decrease at 48 and 72 hours post-transfection (P < 0.0001). CONCLUSION: The findings indicate that targeting SLC16A13 can effectively increase cell death and apoptosis in gastric cancer cells, making it a viable therapeutic target.

Down-regulation and Clinic-pathological Correlation of SIK-1 and SIK-1-LNC in Non-small Cell Lung Cancer Patients

BACKGROUND: Non-small-cell lung cancer (NSCLC) is currently the leading cause of mortality cancer. Introducing noninvasive approaches to diagnose NSCLC, especially at an early phase, might improve the disease's prognosis. Long noncoding RNAs (lncRNAs), which are important regulators of the expression genes inside the cells, have been linked to a range of biological processes, such as cancer progression and metastasis, including NSCLC. The present work aims to determine the potential involvement of SIK-1-LNC and SIK-1 in NSCLC pathogenesis and the possible use of these molecules as novel biomarkers or therapeutic targets. METHODS: In this work, the expression levels of SIK-1-LNC and SIK-1 in 50 pairs of NSCLC tumor and tumor marginal tissues were evaluated. So, after total RNA extraction and complementary DNA synthesis, the SIK-1-LNC and SIK-1 expression levels were evaluated by real-time PCR. In the study groups, clinical and pathological characteristics of the NSCLC patients were also examined. RESULTS: Our findings showed that tumor samples had much lower levels of SIK-1 and SIK-1-LNC expression than tumor margin samples. SIK-1-LNC expression was correlated with SIK-1 levels in NSCLC samples. Interestingly, both stage and lymph node metastasis features of the tumor were associated significantly with SIK-1 and SIK-1-LNC expression levels. A ROC curve analysis indicated a biomarker index of 0.69 and 0.74 for SIK-1 and SIK-1-LNC, respectively. CONCLUSION: Collectively, our study emphasized the role of SIK-1-LNC and SIK-1 downregulation in NSCLC oncogenesis. Additionally, SIK-1 and SIK-1-LNC, particularly the latter, have shown remarkable potential to be utilized as new NSCLC biomarkers and therapeutic targets.

Expression Level of miR-34a in Tumor Tissue from Patients with Esophageal Squamous Cell Carcinoma.

BACKGROUND: miR-34a has been shown to be involved in P53 regulation. In this study, we aimed to evaluate the expression level of miR-34a in esophageal cancer and compare it with that of the normal marginal tissues. METHODS: Tumor and marginal tissues were obtained from 50 patients with esophageal cancer. After RNA extraction, expression level of miR-34a was determined using SYBR green master mix and real-time quantitative PCR. RESULTS: It was observed that there was a downregulation of miR-34a in tumoral tissue of esophageal patients in comparison to normal marginal tissues. Moreover, the expression level of miR-34a was correlated with clinicopathological specifications of the patients. CONCLUSIONS: miR-34a may be involved in the pathogenesis and development of esophageal cancer and have the potential to be used as a diagnostic and therapeutic marker in esophageal cancer.

Expression Level of Caspase Genes in Colorectal Cancer

Background: Caspases proteins are protease enzymes involved in the initiation and execution of apoptosis process. Regulation of apoptosis process plays an important role in the normal biological events and development. In addition to developmental abnormalities, dysregulated apoptosis system may lead to tumorigenesis, autoimmunity, and other serious health problems. Aberrant regulation of apoptosis may also be the paramount cause of chemoresistance during cancer therapy. It is aimed through this study to evaluate the transcript levels of Caspase 3, 8, and 9 in tumoral tissues from patients with colorectal cancer (CRC) and compare it with normal marginal tissues. Methods: Fifty tumor tissues and their matched marginal tissues, as control group, were obtained from CRC patients. Total mRNA of all tissue samples was extracted and cDNA was synthesized. Using SYBR Green PCR master mix and Real-time gene expression technique, the transcript level of target genes was quantified. Results: Experiments indicated that mRNA expressions of caspase 9 and 3 were downregulated in tumoral tissues from CRC patients in comparison to marginal tissues. In contrast, tumoral tissues expressed mRNA of caspase 8 higher than normal marginal tissues. Modified transcript levels of caspase 3, 8, and 9 were correlated with the clinical manifestations of the patients. Conclusions: Alteration in the mRNA level of caspase genes may be involved in the development of CRC.

TP53 Gene Pro72Arg (rs1042522) Single Nucleotide Polymorphism as Not a Risk Factor for Colorectal Cancer in the Iranian Azari Population

Background: The p53 protein participates critically in several cellular functions such as cell growth and DNA repair. Polymorphisms in the TP53 locus have repeatedly been implicated in the pathogenesis of cancers all over the world. Over 200 single nucleotide polymorphisms (SNPs) have been characterized, but one well-known example at at codon 72, Pro72Arg (rs1042522), has the displayed inconsistent results with regard to cancer risk. Herein, we aimed to evaluate whether Pro72Arg (rs1042522) single nucleotide polymorphism (SNP) in TP53 gene might be associated with risk of colorectal cancer in the Iranian Azari population. Methods: Blood samples were taken from 100 healthy controls and 100 colorectal cancer patients with Iranian-Azeri ethnicity. Genotyping was performed with Tetra-ARMS PCR. Results: The alleles of the TP53 gene Pro72Arg SNP did not significantly differ in prevalence between patients and controls (P>0.05). Additionally, genotypes of Pro72Arg SNP were not significantly associated with colorectal cancer risk in the studied population. Conclusions: Pro72Arg SNP of TP53 gene may not be involved in the disease pathogenesis in Iranian Azari patients with colorectal cancer.

The effects of neoadjuvant chemotherapy on resectability of locally-advanced gastric adenocarcinoma: a clinical trial.

INTRODUCTION: Surgical resection is the only curative treatment for gastric cancer. However, the overall prognosis of gastric adenocarcinoma is poor and advanced disease may even make surgical treatment impossible. It has been theoretically proposed that administration of chemotherapy before surgical resection may down-stage the disease state and facilitate resectability especially in locally-advanced tumors. AIM: We wanted to assess the effect of administration of neoadjuvant chemotherapy on tumor resectability in patients with locally-advances gastric adenocarcinoma. MATERIALS AND METHODS: During a randomized-controlled trial, we divided 60 patients with locally-advanced gastric adenocarcinoma into two groups of neoadjuvant chemotherapy and surgery (case) versus surgery alone (control). Because of patient dropouts, we analyzed the results for 22 and 29 patients in case and control groups respectively. The study period was March 21, 2011 to March 20, 2014. A non-randomized set of 23 patients were also added to the control group (Multi-center analysis). The analysis was repeated for non-randomized patients (22 case patients versus 52 control patients). RESULTS: The mean age of patients in case and control groups was 58.3 ± 9.1 and 59.7 ± 8.7 years of age respectively (p > 0.05). Male to female ratio was 15/7 and 41/11 in case and control groups respectively (p > 0.05). In Randomized patients, 19 patients (86.4%) were resectable in case group; while 16 patients (55.2%) were resectable in control group (p < 0.05). Multicenter analysis also revealed resectability in 19 patients (86.4%) and 31 patients (59.6%) of case and control groups respectively (p < 0.05). CONCLUSION: We conclude that neoadjuvant chemotherapy could increase tumor resectability rate in patients with locally-advanced gastric adenocarcinoma. However, further studies are necessary to confirm the effect of this modality on patients' overall survival.