Feng Chen

Gastric cancer is a malignant tumor with a poor prognosis. Therefore, it is important to search for molecules that play a vital role in the development, diagnosis, and treatment of this disease. Placenta‐specific 1 (PLAC1) is one of the cancer‐testis antigens; it plays an important role in both placental development and tumorigenesis. However, the role of PLAC1 in gastric cancer has not been fully investigated, and its underlying mechanism needs further study. We first explored the expression and clinical relevance of PLAC1 in gastric cancer and performed gene set enrichment analysis of PLAC1‐related genes using online databases. Subsequently, we studied the function and mechanism of PLAC1 in gastric cancer cells through in vitro experiments. Our results showed that PLAC1 is highly expressed in gastric cancer, is associated with poor prognosis, and can promote gastric cancer cell proliferation through the AKT/GSK‐3β/cyclin D1 signaling pathway. Moreover, we discovered that AKTi attenuates the effect of PLAC1. Our study further revealed the role and mechanism of PLAC1 in gastric cancer and suggested that this antigen might be a useful molecular marker for gastric cancer diagnosis, prognosis, and treatment.

A 58-year-old female patient came to our hospital for physical examination. CT scan: a round, well-defined and isoechoic nodule has been found in the left adrenal with a clear boundary and scaled about 2.0cm × 1.7 cm. She underwent laparoscopic resection, sequentially occurred complications of the pancreas and renal impairment. Discussion: In general, the accessory spleen is asymptomatic and most were found by ultrasonography in physical examination. Usually, accessory spleen located in the helium or inferior pole of the spleen, rarely in the superior pole or other organs like adrenal. Clinically, it can be misdiagnosed or even caused complications in some serious cases.

The present study aimed to analyze the expression and effects of NUAK2 in gastric cancer and adjacent normal gastric tissues. The protein expression levels of NUAK2 were detected by western blot analysis. The effects of NUAK2 expression on the proliferation of gastric cancer cells was detected using an MTT and BrdU incorporation assay. Furthermore, the effects of NUAK2 on proliferation and cancer stem cell markers, both protein and microRNA (miRNA), were investigated by western blot analysis and miRNA microarrays, respectively. The results demonstrated that NUAK2 was able to significantly promote the proliferation of SGC-7901 gastric cancer cells. In addition, NUAK2 overexpression decreased the percentage of cells in the G1 phase and increased the percentage of cells in the S phase. Western blot analysis and miRNA microarrays revealed that overexpression of NUAK2 resulted in increased expression levels of proliferation markers, including c-myc, proliferating cell nuclear antigen, cyclin-dependent kinase 2, miRNA 21, and gastric cancer stem cell markers, including aldehyde dehydrogenase 1, CD44 and CD133. In conclusion, NUAK2 expression differed between the tumor and normal gastric tissues. NUAK2 was able to promote the proliferation of gastric cancer cells and regulate their cell cycle. Proliferation and cancer stem cell markers were upregulated by NUAK2 expression. Therefore, the results from the present study suggest that NUAK2 may be a promising target for gastric cancer therapy in the future.

MicroRNA-182 (miR-182) is significantly downregulated in human gastric tissue samples. Overexpression of miR-182 suppresses the proliferation and colony formation of gastric cancer cells. However, new aspects of the mechanism are still emerging in gastric cancer. ANUBL1, also known as ZFAND4 (zinc finger, AN1-type domain 4), its roles are scarely reported in cancer. In this study, we not only showed that ANUBL1 as an oncogene was upregulated and could promote proliferation of SGC-7901 cells, but also demonstrated that its over-expression led to a strong decrease of miR-182 expression and expression of ANUBL1 was in turn directly downregulated by miR-182, thereby establishing a negative feedback loop between miR-182 and ANUBL1. The elucidation of the mechanisms of miR-182 targeting ANUBL1 in gastric cancer helps us to further understand the mechanism of gastric cancer initiation and progression.

Membrane type 1 matrix metalloproteinase (MT1-MMP) has been demonstrated to play an important role in tumor progression. The aim of the present study was to analyze the expression of MT1-MMP in breast cancer and its correlation with clinicopathologic characteristics, including the survival of breast cancer patients. In our results, MT-MMP1 was up-expressed in breast cancer tissues compared with ductal hyperplasia tissues in microarray data (GSE2429). MT1-MMP mRNA and protein expression was markedly higher in breast cancer tissues than in normal breast tissues (P=0.005 and P=0.037, respectively). Using immunohistochemistry, high levels of MT1-MMP protein were positively correlated with the status of clinical stage (I-II vs. III-IV; P=0.043), lymph node metastasis (absence vs. presence; P=0.024), and distant metastasis (No vs. Yes; P=0.017) of breast cancer patients. Patients with higher MT1-MMP expression had a significantly shorter overall survival time than did patients with low MT1-MMP expression. Multivariate analysis indicated that the level of MT1-MMP expression was an independent prognostic indicator (P<0.001) for the survival of patients with breast cancer. In conclusions, MT1-MMP plays an important role on breast cancer aggressiveness and prognosis and may act as a promising target for prognostic prediction.

High-mobility group A1 (HMGA1) has been suggested to play a significant role in tumor progression, but little is known about the accurate significance of HMGA1 in non-small cell lung cancer (NSCLC) patients. The aim of this study was to identify the role of HMGA1 in NSCLC. The expression status of HMGA1 was observed initially in NSCLC by Gene Expression Omnibus (GEO). The expression of HMGA1 messenger RNA (mRNA) and protein was examined in NSCLC and adjacent normal lung tissues through real-time PCR and immunohistochemistry. Meanwhile, the relationship of HMGA1 expression levels with clinical features and prognosis of NSCLC patients was analyzed. In our results, HMGA1 was overexpressed in NSCLC tissues compared with adjacent normal lung tissues in microarray data (GSE19804). HMGA1 mRNA and protein expressions were markedly higher in NSCLC tissues than in normal lung tissues (P < 0.001 and P = 0.010, respectively). Using immunohistochemistry, high levels of HMGA1 protein were positively correlated with the status of clinical stage (I–II vs. III–IV, P < 0.001), T classification (T1–T vs. T3–T4, P = 0.003), N classification (N0N1 vs. N2–N3, P < 0.001), M classification (M0 vs. M1, P = 0.002), and differentiated degree (high or middle vs. low or undifferentiated, P = 0.003) in NSCLC. Patients with higher HMGA1 expression had a significantly shorter overall survival time than did patients with low HMGA1 expression. Multivariate analysis indicated that the level of HMGA1 expression was an independent prognostic factor (P < 0.001) for the survival of patients with NSCLC. In conclusion, HMGA1 plays an important role on NSCLC progression and prognosis and may act as a convictive biomarker for prognostic prediction.