AlG3 Induces AURKA to Promote Laryngeal Squamous Cell Carcinoma Metastasis

Objectives To investigate the relationship between ALG3 and AURKA, the expression and potential prognostic value of ALG3 in LSCC, and to then explore the impact of ALG3 in tumorigenic effects.Methods Co-immunoprecipitation assay was detected the relationship between ALG3 and AURKA, Rt-PCR and Western blot was detected the expression of related mRNA and proteins. CCK8 assay, plate colony formation assay Cells, wound healing, migration and invasion assays were used to examine the ability of proliferation, movement, migration and invasion of LSCC cells.Results ALG3 immediately induced AURKA to promote LSCC metastasis. Moreover, ALG3 highly expressed in LSCC tissues and cells and the expression of ALG3 was positively related to tumor size, lymphatic metastasis and poor clinical prognosis. Furthermore, knockdown ALG3 in LSCC cells remarkably restrain cellular proliferation, migration and invasion in vitro and vivo.Conclusion AlG3 induced AURKA to promote LSCC metastasis and ALG3 maybe potential prognostic value for LSCC.Brief AbstractAlG3 induces AURKA to promote laryngeal squamous cell carcinoma metastasis

KIAA1217 Promotes Epithelial-Mesenchymal Transition and Hepatocellular Carcinoma Metastasis by Interacting with and Activating STAT3

The survival and prognosis of hepatocellular carcinoma (HCC) are poor, mainly due to metastasis. Therefore, insights into the molecular mechanisms underlying HCC invasion and metastasis are urgently needed to develop a more effective antimetastatic therapy. Here, we report that KIAA1217, a functionally unknown macromolecular protein, plays a crucial role in HCC metastasis. KIAA1217 expression was frequently upregulated in HCC cell lines and tissues, and high KIAA1217 expression was closely associated with shorter survival of patients with HCC. Overexpression and knockdown experiments revealed that KIAA1217 significantly promoted cell migration and invasion by inducing epithelial-mesenchymal transition (EMT) in vitro. Consistently, HCC cells overexpressing KIAA1217 exhibited markedly enhanced lung metastasis in vivo. Mechanistically, KIAA1217 enhanced EMT and accordingly promoted HCC metastasis by interacting with and activating JAK1/2 and STAT3. Interestingly, KIAA1217-activated p-STAT3 was retained in the cytoplasm instead of translocating into the nucleus, where p-STAT3 subsequently activated the Notch and Wnt/β-catenin pathways to facilitate EMT induction and HCC metastasis. Collectively, KIAA1217 may function as an adaptor protein or scaffold protein in the cytoplasm and coordinate multiple pathways to promote EMT-induced HCC metastasis, indicating its potential as a therapeutic target for curbing HCC metastasis.

Importance of fine needle aspiration cytology in revealing the spectrum of axillary swelling: An experience with 30 cases

FNAC plays an important role in the early diagnosis of the axillary swelling. This study was conducted to document the spectrum of lesions on the patients that came for FNAC with the complain of axillary swelling. Present study was carried out at the Department of Pathology. A total of 30 cases of axillary swelling which were referred for FNAC in the department of Pathology, over the period of 3 months were retrospectively evaluated. All the stained slides of the cases were also reviewed.: From 30 cases there were 13 males and 17 females. On examining the stained slides maximum number of cases presented with chronic granulomatous lymphadenitis followed by Reactive lymphadenitis , Lipoma, Ductal carcinoma metastasis of breast in axillary lymphnode, chronic non-specific lymphadenitis, One unusual case of Hydatid cyst who presenting with axillary swelling was also diagnosed. : FNAC is an important tool in differentiating benign and malignant lesions thus, helps in the proper management of the disease.

Metastatic renal cell carcinoma presenting as a duodenal mass

We report a case of renal cell carcinoma metastasis to the duodenum.

A Case of Solitary Metastatic Deposit in the Orbital Rim from Follicular Thyroid Cancer

Follicular thyroid carcinoma (FTC) is the second most common thyroid cancer, following papillary carcinoma. Metastasis to the orbital rim from FTC is very rare. We recently experienced a case of FTC with metastasis to the orbital rim in a 74-year-old woman, who initially presented with a huge thyroid mass and an asymptomatic solitary orbital rim lesion. The solitary orbital rim lesion was suspected to be a separate disease entity such as lymphoma from the preoperative imaging, but bone metastasis from FTC was finally confirmed after orbital rim resection and total thyroidectomy. During follow-up, the patient presented multiple bone metastasis, so the solitary orbital rim lesion was considered a clinical sign of systemic metastasis from FTC. Therefore, we present this unique case with a review of the literature.

ONECUT2 facilitates hepatocellular carcinoma metastasis by transcriptionally upregulating FGF2 and ACLY

Metastasis is the predominant reason for high mortality of hepatocellular carcinoma (HCC) patients. It is critical to explore the molecular mechanism underlying HCC metastasis. Here, we reported that transcription factor One Cut homeobox 2 (ONECUT2) functioned as an oncogene to facilitate HCC metastasis. Elevated ONECUT2 expression was positively correlated with increased tumor number, tumor encapsulation loss, microvascular invasion, poor tumor differentiation, and advanced TNM stage. Mechanistically, ONECUT2 directly bound to the promoters of fibroblast growth factor 2 (FGF2) and ATP citrate lyase (ACLY) and transcriptionally upregulated their expression. Knockdown of FGF2 and ACLY inhibited ONECUT2-mediated HCC metastasis, whereas upregulation of FGF2 and ACLY rescued ONECUT2 knockdown-induced suppression of HCC metastasis. ONECUT2 expression was positively correlated with FGF2 and ACLY expression in human HCC tissues. HCC patients with positive coexpression of ONECUT2/FGF2 or ONECUT2/ACLY exhibited the worst prognosis. In addition, FGF2 upregulated ONECUT2 expression through the FGFR1/ERK/ELK1 pathway, which formed an FGF2-FGFR1-ONECUT2 positive feedback loop. Knockdown of ONECUT2 inhibited FGF2-induced HCC metastasis. Furthermore, the combination of FGFR1 inhibitor PD173074 with ACLY inhibitor ETC-1002 markedly suppressed ONECUT2-mediated HCC metastasis. In summary, ONECUT2 was a potential prognostic biomarker in HCC and targeting this oncogenic signaling pathway may provide an efficient therapeutic strategy against HCC metastasis.