China
Africa
Explore chapters and articles related to this topic
*
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
*
Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
Atmospheric aging increases the cytotoxicity of bare soot particles in BEAS-2B lung cells
Published in Aerosol Science and Technology, 2023
Michal Pardo, Hendryk Czech, Svenja Offer, Martin Sklorz, Sebastiano Di Bucchianico, Elena Hartner, Jana Pantzke, Evelyn Kuhn, Andreas Paul, Till Ziehm, Zhi-Hui Zhang, Gert Jakobi, Stefanie Bauer, Anja Huber, Elias J. Zimmermann, Narges Rastak, Stephanie Binder, Ramona Brejcha, Eric Schneider, Jürgen Orasche, Christopher P. Rüger, Thomas Gröger, Sebastian Oeder, Jürgen Schnelle-Kreis, Thorsten Hohaus, Markus Kalberer, Olli Sippula, Astrid Kiendler-Scharr, Ralf Zimmermann, Yinon Rudich
DNA damage can often results in cell cycle alterations, a series of events that govern cell replication and division (Chatterjee and Walker 2017; Shaltiel et al. 2015). An increased expression of p16, a known cell cycle marker, was observed, particularly in cells exposed to aged-SP (Figure 6d). To the same extent, exposure to fresh- or aged-SP statistically increased p21 compared to the CA control (Figure 6e). p16 inhibits cyclin-dependent kinase (CDK) and cell cycle progression from the G1/S phase, and p21 arrests the cell cycle progression in G1/S and G2/M (Li et al. 2021b). Therefore, it is suggested that fresh- and aged-SP influence the cell cycle at the G1/S checkpoint, preventing cells from entering the S phase, as only the p16 levels were influenced in this study. This is in accordance with a previous study showing that combustion-derived particles from wood pellet burning induced DNA damage and cell cycle alterations by accumulating cells in the S/G2 phase (Marchetti et al. 2021). Furthermore, p21 intricate network and multiple activities can act as an oncogenic protein or tumor suppressor (Shaltiel et al. 2015). Nevertheless, exposure to PAH increased p21 in vitro (Li et al. 2021a; Park et al. 2021) and in vivo (Saleh et al. 2022), supporting our observation of the involvement of p21.