Proliferation Independent Activation of Programmed Cell Death as a Novel Therapy for Prostate Cancer

Apoptosis ◽  
1994 ◽  
pp. 137-155 ◽  
Author(s):  
Yuzo Furuya ◽  
Richard S. Berges ◽  
Per Lundmo ◽  
John T. Isaacs
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Novel Therapy

Cytotoxicity of obacunone and obacunone glucoside in human prostate cancer cells involves Akt-mediated programmed cell death

Toxicology ◽  
2015 ◽  
Vol 329 ◽  
pp. 88-97 ◽  
Author(s):  
Kotamballi N. Chidambara Murthy ◽  
Guddadarangavvanahally K. Jayaprakasha ◽  
Bhimanagouda S Patil
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Resveratrol-loaded PLGA nanoparticles mediated programmed cell death in prostate cancer cells

2018 ◽  
Vol 26 (6) ◽  
pp. 876-885 ◽  
Author(s):  
Anmar M. Nassir ◽  
Naiyer Shahzad ◽  
Ibrahim A.A. Ibrahim ◽  
Iqbal Ahmad ◽  
Shadab Md ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Plga Nanoparticles ◽  
Prostate Cancer Cells

scholarly journals Rare sugar d-allose induces programmed cell death in hormone refractory prostate cancer cells

APOPTOSIS ◽  
2009 ◽  
Vol 14 (7) ◽  
pp. 926-927 ◽  
Author(s):  
Nibedita Naha ◽  
Hae Young Lee ◽  
Mi Ja Jo ◽  
Bong Chul Chung ◽  
Sung Hoon Kim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Hormone Refractory Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Rare Sugar ◽  
Hormone Refractory

Reduced Expression of Programmed Cell Death 5 Protein in Tissue of Human Prostate Cancer

2009 ◽  
Vol 24 (4) ◽  
pp. 241-245 ◽  
Author(s):  
Yue-jun Du ◽  
Lin Xiong ◽  
Yan Lou ◽  
Wan-long Tan ◽  
Shao-bin Zheng
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Programmed Cell Death 5

scholarly journals Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
YouZhi Wang ◽  
Ning Wu ◽  
Ning Jiang
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Bone Metastasis ◽  
Programmed Cell Death ◽  
Pathologic Fracture ◽  
Resistance Mechanisms ◽  
The Body ◽  
Prostate Cancer Treatment ◽  
Multiple Organs ◽  
Important Marker

AbstractProstate cancer is a common malignant tumor, which can spread to multiple organs in the body. Metastatic disease is the dominant reason of death for patients with prostate cancer. Prostate cancer usually transfers to bone. Bone metastases are related to pathologic fracture, pain, and reduced survival. There are many known targets for prostate cancer treatment, including androgen receptor (AR) axis, but drug resistance and metastasis eventually develop in advanced disease, suggesting the necessity to better understand the resistance mechanisms and consider multi-target medical treatment. Because of the limitations of approved treatments, further research into other potential targets is necessary. Metastasis is an important marker of cancer development, involving numerous factors, such as AKT, EMT, ECM, tumor angiogenesis, the development of inflammatory tumor microenvironment, and defect in programmed cell death. In tumor metastasis, programmed cell death (autophagy, apoptosis, and necroptosis) plays a key role. Malignant cancer cells have to overcome the different forms of cell death to transfer. The article sums up the recent studies on the mechanism of bone metastasis involving key regulatory factors such as macrophages and AKT and further discusses as to how regulating autophagy is crucial in relieving prostate cancer bone metastasis.

Defining the regulatory role of programmed cell death 4 in laryngeal squamous cell carcinoma

2018 ◽  
Vol 96 (5) ◽  
pp. 522-538 ◽  
Author(s):  
Yuan-Teng Xu ◽  
Rui-Qing Chen ◽  
Gong-Biao Lin ◽  
Xiu-Ling Fang ◽  
Shu-Juan Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Laryngeal Carcinoma ◽  
Malignant Tumors ◽  
Clinical Stage ◽  
Regulatory Relationship ◽  
Novel Therapy ◽  
Programmed Cell Death 4 ◽  
E Cadherin

Programmed cell death 4 (PDCD4) is decreased in many different kinds of malignant tumors. EMT endows tumor cells invasive and metastatic properties. However, few studies have determined the role of PDCD4 in the regulation of EMT in the context of laryngeal carcinoma. We examined the relationship between PDCD4 and EMT-associated proteins E-cadherin and N-cadherin using laryngeal carcinoma tissues. Gene manipulation was used to define the regulatory capacity of PDCD4. We report that PDCD4 and E-cadherin/N-cadherin expression were significantly changed in the carcinoma tissues, and their expression was associated with pathological grade, metastatic state, and clinical stage. The suppression of PDCD4 (and consequently, E-cadherin) was concomitant with increased proliferation and G2-phase arrest, decreased apoptosis, and increased cell invasion. PDCD4 upregulation reversed the above-mentioned results. In nude mice, PDCD4 knockdown increased tumor growth and pathological features, confirming the tumorigenic role of PDCD4. Finally, PDCD4 silencing was associated with dysregulation of the carcinogenic Wnt–β-catenin and the STAT3–miR-21 signaling pathways. This study revealed a dynamic regulatory relationship between PDCD4 and critical factors for EMT, establishing a broad, functional role for PDCD4 in laryngeal carcinoma, which may be propagated by the STAT3–miR-21 pathway. These findings provide new information on an EMT-associated target that may lead to a novel therapy.

Sign in / Sign up

Export Citation Format

Share Document