ABSTRACT
Objective: Clarify the expression changes, biological functions and related mechanisms of long non-coding RNA (lncRNA) ZEB2-AS1 in colon cancer tissues. Methods: The expression levels of ZEB2-AS1 in colon cancer tissues and adjacent tissues were detected by qRT-PCR and in situ hybridization methods. Cell biology experiments were performed to detect the proliferation, migration and apoptosis of colon cancer cells when the level of ZEB2-AS1 was overexpression or silencing. Then, Western blot was performed to analyze the effect of ZEB2-AS1 on the expression levels of ß-catenin protein and related genes in the signal pathway. Results: We found that the expression level of ZEB2-AS1 in colon cancer tissues was significantly up-regulated compared with that in adjacent normal tissues. In colon cancer cell line of HCT8, overexpression of ZEB2-AS1 could promote cell proliferation and migration, while silencing ZEB2-AS1 would enhance cell apoptosis and inhibit proliferation. Study on the mechanism of ZEB2-AS1 showed that it could promote the expression of ß-catenin, activate downstream genes to be transcribed and promote the occurrence and development of tumors. Conclusion: ZEB2-AS1 could promote colon cancer cell proliferation and inhibit apoptosis to promote the progression of colon cancer by upregulating the expression of ß-catenin protein. ZEB2-AS1 may be a useful new target for treating colon cancer patients.
Subject(s)
Colonic Neoplasms/genetics , Gene Expression Regulation, Neoplastic , Oligonucleotides, Antisense/genetics , RNA, Long Noncoding/genetics , Zinc Finger E-box Binding Homeobox 2/genetics , Apoptosis , Biomarkers, Tumor , Cell Line, Tumor , Cell Movement , Cell Proliferation , Gene Expression Profiling , Gene Silencing , Humans , Signal Transduction , beta Catenin/geneticsABSTRACT
Lung cancer is a common malignancy in the world; however symptomatic colonic metastasis from primary lung cancer is rare. A 64-year-old man was originally found poorly differentiated squamous cell carcinoma of right lung and received right lower lobectomy and lymph node dissection. Three years later, the patient presented to our emergency room with the symptom of upper abdominal pain and weight loss. Abdominal palpation and computed tomography scan of the abdomen revealed a large mass measuring 7.6 cm × 8.5 cm in the ascending colon. Colonoscopy and biopsy revealed poorly differentiated squamous cell carcinoma with similar morphological pattern to that of the previous lung cancer. Chemotherapy was given and the patient died 5 mo later. Lung cancer metastatic to the colon confers a poor prognosis: overall survival ranged from 5 wk to 1 year, with a median survival of 3 mo after the diagnosis of the colonic metastasis.
Subject(s)
Carcinoma, Squamous Cell/pathology , Carcinoma, Squamous Cell/surgery , Colonic Neoplasms/diagnosis , Colonic Neoplasms/secondary , Lung Neoplasms/pathology , Lung Neoplasms/surgery , Antineoplastic Agents/therapeutic use , Cell Differentiation , Colonic Neoplasms/drug therapy , Colonoscopy , Diagnosis, Differential , Fatal Outcome , Humans , Male , Middle Aged , Neoplasm Metastasis , Treatment OutcomeABSTRACT
Pancreatic cancer has one of worst prognosis among all human malignancies around the world, the development of novel and more efficient anti-cancer agents against this disease is urgent. In the current study, we tested the potential effect of INK-128, a novel mammalian target of rapamycin (mTOR) complex 1 and 2 (mTORC1/2) dual inhibitor, against pancreatic cancer cells in vitro. Our results demonstrated that INK-128 concentration- and time-dependently inhibited the survival and growth of pancreatic cancer cells (both primary cells and transformed cells). INK-128 induced pancreatic cancer cell apoptosis and necrosis simultaneously. Further, INK-128 dramatically inhibited phosphorylation of 4E-binding protein 1 (4E-BP1), ribosomal S6 kinase 1 (S6K1) and Akt at Ser 473 in pancreatic cancer cells. Meanwhile, it downregulated cyclin D1 expression and caused cell cycle arrest. Finally, we found that a low concentration of INK-128 significantly increased the sensitivity of pancreatic cancer cells to gemcitabine. Together, our in vitro results suggest that INK-128 might be further investigated as a novel anti-cancer agent or chemo-adjuvant for pancreatic cancer treatment.
Subject(s)
Adenocarcinoma/pathology , Antineoplastic Agents/pharmacology , Benzoxazoles/pharmacology , Multiprotein Complexes/antagonists & inhibitors , Pancreatic Neoplasms/pathology , Pyrimidines/pharmacology , TOR Serine-Threonine Kinases/antagonists & inhibitors , Adult , Apoptosis/drug effects , Cell Line, Transformed , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Deoxycytidine/analogs & derivatives , Deoxycytidine/pharmacology , Drug Synergism , Humans , Male , Mechanistic Target of Rapamycin Complex 1 , Mechanistic Target of Rapamycin Complex 2 , Necrosis , GemcitabineABSTRACT
OBJECTIVE: To investigate the therapeutic efficacy and adverse reactions of Aidi Injection (AI) combined with percutaneous cool-tip radiofrequency ablation (CRFA) in treatment of primary liver cancer and to explore its effect on immune function. METHODS: Eighty-nine patients with primary liver cancer at middle-late stage were assigned to the control group with CRFA alone and the treatment group treated with CRFA and intravenous dripping of AI 50 mL once every day for succesive 20 days. RESULTS: Compared with those before treatment, the alanine aminotransferase (ALT) and albumin (ALB) levels showed no marked change, and CD4 subgroup of T lymphocyte and CD4/CD8 ratio elevated in the treatment group (P<0.01), while the ALT level elevated (P<0.05), ALB level decreased (P < 0.01), CD4 and CD4/CD8 ratio showed no change in the control group. The relapse rate was 20.0% (3/15) in patients with tumor more than 3 cm in diameter of the treatment group, which was obvious lower than that in the control group (55.0%, 11/20, P < 0.05). CONCLUSION: AI treatment could relieve the impairment of CRFA on hepatic function, improve immune function and reduce relapse rate in patients with primary liver cancer.