Squamous cell carcinoma of the cystic duct: A case report and literature review.

RATIONALE: Pure squamous cell carcinoma (SCC) of the gallbladder is a rare malignant biliary tract tumor predominantly found in the body and neck of the gallbladder. However, its occurrence in the cystic duct is even rarer. Given its rarity, no established guidelines or consensus currently exist regarding the treatment of pure SCC of the gallbladder. We report an unusual case of SCC originating from the cystic duct with the intent of providing insights into the therapeutic approach for this type of malignancy. PATIENT CONCERNS: A male patient presented to our hospital with acute cholecystitis. Unexpectedly, imaging revealed gallbladder malignancy. DIAGNOSES: Pathologic examination after surgery confirmed SCC of the cystic duct. INTERVENTIONS: Despite elevated bilirubin levels, we were able to exclude hilar involvement, enabling radical tumor resection. Intraoperatively, we discovered that the tumor was located in the cystic duct, a site associated with a high likelihood of invasion into neighboring organs. The tumor demonstrated a predominantly exophytic growth pattern, which prompted us to refrain from extending the resection range, thereby striking a balance between complete tumor removal and surgical trauma. We performed liver wedge resection only to ensure a negative resection margin while preserving the anatomical structure to the greatest extent possible. Postoperative recovery was rapid and uncomplicated. Pathological examination confirmed pure SCC, which led us to initiate a regimen of nab-paclitaxel and cisplatin, which is known to be effective in other organ SCCs. Remarkably, the patient experienced a rare and severe posttreatment cardiovascular event. Consequently, we switched the patient to a chemotherapy regimen of gemcitabine and cisplatin, which ultimately yielded positive clinical outcomes. OUTCOMES: no evidence of tumor recurrence was observed within 1 year after surgery. LESSONS: The diagnosis and therapeutic strategy for rare tumors such as gallbladder SCC should be meticulously tailored based on their unique characteristics to optimize postoperative patient outcomes.

Long non-coding RNA TUSC7 suppressed colorectal cancer progression via regulation of miR-23b/PDE7A Axis.

PURPOSE: Despite advances in our understanding of the roles of the long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) in cancer biology, which has been identified to act as a tumor suppressor by regulating cell proliferation, apoptosis, migration, invasion, cell cycle and tumor growth, its function in colorectal cancer remains unknown. METHODS: The expression levels of TUSC7 in colorectal cancer tissues and cell lines were determined, and the biological functions of TUSC7 to cancer progression in colorectal cancer were investigated via correlation analysis of clinical samples, cell viability assay, transwell assay and apoptosis analysis. Further, the molecular regulatory mechanisms of TUSC7 were demonstrated by luciferase reporter assay and western blotting. RESULTS: We observed that the expression of TUSC7 was markedly decreased in colorectal cancer cell lines. Moreover, the lower expression of TUSC7 was correlated with advanced clinical grades and poorer survival and may be an independent risk factor for colorectal cancer. Moreover, the expression of TUSC7 inhibited cell proliferation, invasion and epithelial-to-mesenchymal transition (EMT), while it facilitated apoptosis through competitively binding miR-23b. We also found that TUSC7 decreased the expression of phosphodiesterase 7A (PDE7A), a downstream target of miR-23b, through the TUSC7/miR-23b/PDE7A axis. CONCLUSION: We demonstrated the expression of TUSC7 suppressed colorectal cancer progression through the TUSC7/miR-23b/PDE7A axis, suggesting that TUSC is a potential target for therapeutic intervention in colorectal cancer.

MiR-23b inhibits cell migration and invasion through targeting PDE7A in colon cancer cells.

It has been found that the abnormal expression of miR-23b is related to the poor prognosis or the weak ability of metastasis in colorectal cancer. Furthermore, high expression of PDE7A in tumors is known to be related to poor prognosis. The aim of this study was to explain whether miR-23b was involved in the invasion and metastasis of colon cancer by regulating PDE7A gene. The expression levels of miR-23b and PDE7A in colon tissues and colon cancer cell lines (SW620 and SW480 cells) were measured by real time PCR. The PDE7A protein level was determined by Western blotting. The relationship between miR-23b and PDE7A was verified by cell transfection and luciferase reporter assay. The effect of miR-23b or PDE7A level on cell invasion and migration was determined by Transwell assay. miR-23b was down-regulated when PDE7A was up-regulated in colon cancer tissues and cells. The result of dual luciferase reporter assay showed that PDE7A was a direct target gene of miR-23b. Overexpression of miR-23b not only reduced the expression of PDE7A in SW620 cells or SW480 cells, but also weakened the migration and invasion abilities of SW620 cells or SW480 cells. When SW620 cells or SW480 cells were transfected with si-PDE7A, the level of PDE7A increased and the migration and invasion abilities of cells diminished. In conclusion, miR-23b is lowly expressed in colon cancer tissues and cells, and miR-23b may play an inhibitory role in the development of colon cancer through down-regulating the expression of PDE7A.