2014Oncology ReportsOpen access

BMP8B mediates the survival of pancreatic cancer cells and regulates the progression of pancreatic cancer

Zhuoxin Cheng, Wu Cui, Ye Ding, Tao Liu, Weixin Liu, Youyou Qin, Wei-Bin Xia, Jian Xu, Yinghai Zhang, Xiaoming Zou

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Abstract

Pancreatic cancer has become one of the most common types of cancer. It is believed that inhibiting the apoptosis of tumor cells as well as overgrowth of tumor cells accelerate the progression and development of cancer. However, the detailed mechanisms of pancreatic cancer progression remain to be fully elucidated. Although bone morphogenetic protein (BMP) families are crucial mediators in some types of cancer, whether BMP8B is involved in regulating the growth and apoptosis of pancreatic cancer cells and the progression of pancreatic cancer is not clear. In the present study, we found that the expression of BMP8B was downregulated in pancreatic cancer tissue compared with the normal tissue adjacent to the tumors. Moreover, the overexpression of BMP8B inhibited cell growth and promoted activation of caspase-3 and -9, the decrease of mitochondrial membrane potential and cell apoptosis in PANC-1, while silencing the BMP8B gene expression with BMP8B shRNA exerted anti-apoptotic effects and boosted the growth of pancreatic cancer cells in BxPC-3. Therefore, we concluded that BMP8B mediates the survival of pancreatic cancer cells and regulates the progression of pancreatic cancer, making it a potential therapeutic target for pancreatic cancer.

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Pancreatic cancer has become one of the most common types of cancer. It is believed that inhibiting the apoptosis of tumor cells as well as overgrowth of tumor cells accelerate the progression and development of cancer. However, the detailed mechanisms of pancreatic cancer progression remain to be fully elucidated. Although bone morphogenetic protein (BMP) families are crucial mediators in some types of cancer, whether BMP8B is involved in regulating the growth and apoptosis of pancreatic cancer cells and the progression of pancreatic cancer is not clear. In the present study, we found that the expression of BMP8B was downregulated in pancreatic cancer tissue compared with the normal tissue adjacent to the tumors. Moreover, the overexpression of BMP8B inhibited cell growth and promoted activation of caspase-3 and -9, the decrease of mitochondrial membrane potential and cell apoptosis in PANC-1, while silencing the BMP8B gene expression with BMP8B shRNA exerted anti-apoptotic effects and boosted the growth of pancreatic cancer cells in BxPC-3. Therefore, we concluded that BMP8B mediates the survival of pancreatic cancer cells and regulates the progression of pancreatic cancer, making it a potential therapeutic target for pancreatic cancer.

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Available abstract

Pancreatic cancer has become one of the most common types of cancer. It is believed that inhibiting the apoptosis of tumor cells as well as overgrowth of tumor cells accelerate the progression and development of cancer. However, the detailed mechanisms of pancreatic cancer progression remain to be fully elucidated. Although bone morphogenetic protein (BMP) families are crucial mediators in some types of cancer, whether BMP8B is involved in regulating the growth and apoptosis of pancreatic cancer cells and the progression of pancreatic cancer is not clear. In the present study, we found that the expression of BMP8B was downregulated in pancreatic cancer tissue compared with the normal tissue adjacent to the tumors. Moreover, the overexpression of BMP8B inhibited cell growth and promoted activation of caspase-3 and -9, the decrease of mitochondrial membrane potential and cell apoptosis in PANC-1, while silencing the BMP8B gene expression with BMP8B shRNA exerted anti-apoptotic effects and boosted the growth of pancreatic cancer cells in BxPC-3. Therefore, we concluded that BMP8B mediates the survival of pancreatic cancer cells and regulates the progression of pancreatic cancer, making it a potential therapeutic target for pancreatic cancer.

Key concepts: Pancreatic cancer, Cancer, Oncogene, Cancer research, Gene silencing, Cancer cell, Apoptosis, Cell cycle

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