An-Najah Candidate to Japan Helps in Inventing a New Treatment Strategy for Melanoma
Dr. Yousef Salameh is one of the Biotechnology Department graduates of An-Najah's Faculty of Science who graduated in 2009. He is also An-Najah candidate to Japan for his PhD studies since 2012.
During his study years in Japan, he became interested in cancer and stem cells discipline, and now he is one of the best researchers in this field not only in Japan but also globally.
Recently, he and a research team from the Institute of Medical Science at the University of Tokyo were able to invent a new treatment strategy for Melanoma.
Melanoma, also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes. Melanomas typically occur in the skin, but may rarely occur in the mouth, intestines, or eye. Recently, he and a team of researchers from the Institute of Medical Science at the University Of Tokyo were able to invent a new mechanism for Melanoma treatment.
The research titled: "The fibrinolytic factor tPA drives LRP1-mediated melanoma growth and metastasis" says that the multifunctional endocytic receptor low-density lipoprotein receptor-related protein (LRP)1 has recently been identified as a hub within a biomarker network for multicancer clinical outcome prediction. The mechanism how LRP1 modulates cancer progression is poorly understood.
The study finds that LRP1 and one of its ligands, tissue plasminogen activator (tPA), are expressed in melanoma cells and control melanoma growth and lung metastasis in vivo. Mechanistic studies were performed on 2 melanoma cancer cell lines, B16F10 and the B16F1 cells, both of which form primary melanoma tumors, but only B16F10 cells metastasize to the lungs. Tumor-, but not niche cell–derived tPA, enhanced melanoma cell proliferation in tPA−/− mice. Gain-of-function experiments revealed that melanoma LRP1 is critical for tumor growth, recruitment of mesenchymal stem cells into the tumor bed, and metastasis.
Melanoma LRP1 was found to enhance ERK activation, resulting in increased matrix metalloproteinase (MMP)-9 RNA, protein, and secreted activity, a well-known modulator of melanoma metastasis. Restoration of LRP1 and tPA in the less aggressive, poorly metastatic B16F1 tumor cells enhanced tumor cell proliferation and led to massive lung metastasis in murine tumor models. Antimelanoma drug treatment induced tPA and LRP1 expression.
tPA or LRP1 knockdown enhanced chemosensitivity in melanoma cells. The results identify the tPA-LRP1 pathway as a key switch that drives melanoma progression, in part by modulating the cellular composition and proteolytic makeup of the tumor niche.
Targeting this pathway may be a novel treatment strategy in combination treatments for melanoma. tPA drives LRP1-mediated melanoma growth and metastasis.
It is worth mentioning that the research was published by the FASEB Journal, a scientific journal related to experimental biosciences, promoting scientific progress and education.
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