Expression of KLF9 in pancreatic cancer and its effects on the invasion, migration, apoptosis, cell cycle distribution, and proliferation of pancreatic cancer cell lines

Abstract

Kruppel-like factor 9 (KLF9), a transcription factor, is critical for the inhibition of growth and development of tumors, whereas its effects in pancreatic cancer remains unclear. The purpose of the present study was to investigate the expression and functional significance of KLF9 in vitro, by assessing the expression of KLF9 in pancreatic cancer tissue samples and its association with the total survival of patients and clinicopathological data. The levels of KLF9 expression in adjacent tissues and pancreatic cancer tissues were detected using immunohistochemistry. Using western blot analyses, we assessed KLF9 expression in human pancreatic cancer cell lines. Using flow cytometric analysis and CCK-8, we evaluated the effects of KLF9 expression on cell apoptosis, the cell cycle and proliferation of pancreatic cancer cells. Its effects on migration and cell invasion were detected by performing Transwell assay. By conducting western blot analyses, we evaluated the expression of relative target proteins (involved in invasion, migration, apoptosis, and cell cycle distribution. Our results revealed that in both tissue samples and cell lines (particularly in BxPC-3 and PANC-1 cells) of pancreatic cancer, KLF9 exhibited relatively lower expression. In addition, low KLF9 expression was related to the differentiation (P<0.001) and depth of vascular invasion (P=0.016) and was associated with a poor overall survival rate. In PANC-1 and BxPC-3 cells, KLF9 overexpression decreased the proliferation of pancreatic cancer cells, induced apoptosis, blocked the cell cycle at the S phase, and inhibited the migration and invasion of tumor cells. KLF9 overexpression downregulated MMP-9, MMP-2 Bcl-2, N-cadherin and cyclin B, and upregulated the levels of E-cadherin, Bax, p53, CDK4 and cyclin D1. On the whole, our findings indicated that KLF9 exhibited low expression in pancreatic cancer, and upregulation of KLF9 may inhibit the progression of pancreatic cancer. KLF9 may have potential diagnostic and therapeutic values in this type of cancer.

Dexamethasone induces aberrant macrophage immune function and apoptosis

“…Although various modes of action are still debated, it is broadly accepted that GCs mediate their anti-inflammatory and immunosuppressive effects by affecting macrophage viability and antitumor functionality (4). Several studies have demonstrated that tumor-derived KLF9 may act as a tumor suppressor by promoting apoptosis (8,19,20). Decreased KLF9 suppresses oxidative stress and apoptosis, subsequently promoting cancer progression (7).…”

“…Krüppel-like factor 9 (KLF9), also called basic transcription element-binding protein-1 (Bteb1), is a ubiquitously expressed member of the C2H2-type zinc finger family (7). A recent study suggested that KLF9 plays an important role in regulating animal development and differentiation of various cell types (8). KLF9 can be induced by several physiological or pathological stresses.…”

Long non‑coding RNA TP73‑AS1 accelerates the progression and cisplatin resistance of non‑small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA‑34a‑5p

“…Aberrant increased or decreased expression of miRNAs has been implicated in different human diseases, particularly cancer ( 16 ). Previous studies demonstrated that miR-34a-5p acted as a tumor suppressor in various types of cancer, such as colorectal cancer ( 17 ), cervical cancer ( 18 ) and pancreatic carcinoma ( 19 ). However, the role of miR-34a-5p in lung cancer is unknown.…”

Study on mRNA expression of Cajal body – Gemini of coiled body proteins in head and neck squamous cell carcinoma

“…KLF9 role is notable in lung and pancreas tumors. [46] The role of these genes in HNSCC remains to be explored.…”