Phycocyanin isolated from marine organisms has the characteristics of high efficiency and low toxicity, and it can be used as a functional food. It has been reported that phycocyanin has anti-oxidative function, anti-inflammatory activity, anti-cancer function, immune enhancement function, liver and kidney protection pharmacological effects. Thus, phycocyanin has an important development and utilization as a potential drug, and phycocyanin has become a new hot spot in the field of drug research. So far, there are more and more studies have shown that phycocyanin has the anti-cancer effect, which can block the proliferation of cancer cells and kill cancer cells. Phycocyanin exerts anti-cancer activity by blocking tumor cell cell cycle, inducing tumor cell apoptosis and autophagy, thereby phycocyanin can serve as a promising anti-cancer agent. This review discusses the therapeutic use of phycocyanin and focuses on the latest advances of phycocyanin as a promising anti-cancer drug.

BackgroundTriple-negative breast cancer is a biological subtype of breast cancer, which is unresponsive to conventional chemotherapies and has a poor prognosis. C-Phycocyanin (C-PC), a marine natural purified from Spirulina platensis, has been investigated that has anti-cancer function. The mitogen activated protein kinase (MAPK) pathway plays a crucial role in the development and progression of cancer. Therefore, we would like to study the anti-cancer effects of C-phycocyanin in the treatment of triple-negative breast cancer, and explore the role of MAPK pathway in the anti-tumor effects of C-phycocyanin.MethodsCell proliferation, cell cycle, cell apoptosis and cell migration were explored in breast cancer MDA-MB-231 cell lines. AKT, MAPK and membrane death receptor signaling were evaluated in MDA-MB-231 cell lines.ResultsOur study indicated that C-phycocyanin inhibited cell proliferation and reduced colony formation ability of MDA-MB-231 cells. Furthermore, C-phycocyanin induced cell cycle G0/G1 arrest by decreasing protein expression levels of Cyclin D1 and CDK-2 and increasing protein expression levels of p21 and p27. In addition, C-phycocyanin induced cell apoptotic by activating cell membrane surface death receptor pathway. Besides, C-phycocyanin down-regulated the protein expression levels of cyclooxygenase-2, and further inhibited MDA-MB-231 cells migration. We also found cell death induced by C-phycocyanin was carried through the MAPK signaling pathways. C-Phycocyanin was able to induce MDA-MB-231 cell apoptosis by activating p38 MAPK and JNK signaling pathways while inhibiting ERK pathway.ConclusionsC-Phycocyanin exerted anti-cancer activity via the MAPK signaling pathway in MDA-MB-231 cells.

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We experimentally investigate the drag modification by neutrally buoyant finite-size particles with various aspect ratios in a Taylor–Couette (TC) turbulent flow. The current Reynolds number, $Re$ , ranges from $6.5\times 10^3$ to $2.6\times 10^4$ , and the particle volume fraction, $\varPhi$ , is up to $10\,\%$ . Particles with three kinds of aspect ratio, $\lambda$ , are used: $\lambda =1/3$ (oblate), $\lambda =1$ (spherical) and $\lambda =3$ (prolate). Unlike the case of bubbly TC flow (van Gils et al., J. Fluid Mech., vol. 722, 2013, pp. 317–347; Verschoof et al., Phys. Rev. Lett., vol. 117, issue 10, 2016, p. 104502), we find that the suspended finite-size particles increase the drag of the TC system regardless of their aspect ratios. The overall drag of the system increases with increasing $Re$ , which is consistent with the literature. In addition, the normalized friction coefficient, $c_{f,\varPhi }/c_{f,\varPhi =0}$ , decreases with increasing $Re$ , the reason could be that in the current low volume fractions the turbulent stress becomes dominant at higher $Re$ . The particle distributions along the radial direction of the system are obtained by performing optical measurements at $\varPhi =0.5\,\%$ and $\varPhi = 2\,\%$ . As $Re$ increases, the particles distribute more evenly in the entire system, which results from both the greater turbulence intensity and the more pronounced finite-size effects of the particles at higher $Re$ . Moreover, it is found that the variation of the particle aspect ratios leads to different particle collective effects. The suspended spherical particles, which tend to cluster near the walls and form a particle layer, significantly affect the boundary layer and result in maximum drag modification. The minimal drag modification is found in the oblate case, where the particles preferentially cluster in the bulk region, and, thus, the particle layer is absent. Based on the optical measurement results, it can be concluded that, in the low volume fraction ranges ( $\varPhi =0.5\,\%$ and $\varPhi = 2\,\%$ here), the larger drag modification is connected to the near-wall particle clustering. The present findings suggest that the particle shape plays a significant role in drag modification, and the collective behaviours of rigid particles provide clues to understand the bubbly drag reduction.

The remarkable ability of a new dinuclear Ru (II) complex Ru 2(obip)L 4 [obip = 2-(2-pyridyl)imidazo[4,5- f][1,10]-phenanthroline; L = 2,2'-bipyridine] to promote the formation and stabilization of the human telomeric repeat AG3(T2AG3)3 quadruplex was reported. The experimental results indicated that Ru 2(obip)L 4 could induce the formation of an antiparallel G-quadruplex structure in the absence of metal cations. It could induce positive T m shifts of +9.4 and +5.8 degrees C in Na (+) and K (+) buffers, respectively, in which an increase in the melting temperature of the quadruplex indicated a stabilizing effect. Binding stoichiometry with the quadruplex was investigated through a luminescence-based Job plot. The major inflection point for Ru 2(obip)L 4 at x = 0.48 was observed. The data were consistent with a 1:1 [quadruplex]/[complex] binding mode, which was suggestive of a specific Ru 2(obip)L 4-quadruplex interaction with a single guanine tetrad.

CUL4B, a scaffold protein that assembles the CRL4B ubiquitin ligase complex, participates in the regulation of a broad spectrum of biological processes. Here, we demonstrate a crucial role of CUL4B in driving cell cycle progression. We show that loss of CUL4B results in a significant reduction in cell proliferation and causes G1 cell cycle arrest, accompanied by the upregulation of the cyclindependent kinase (CDK) inhibitors (CKIs) p21 and p57 (encoded by CDKN1A and CDKN1C, respectively). Strikingly, CUL4B was found to negatively regulate the function of p21 through transcriptional repression, but not through proteolysis. Furthermore, we demonstrate that CRL4B and SIN3A-HDAC complexes interact with each other and co-occupy the CDKN1A and CDKN1C promoters. Lack of CUL4B led to a decreased retention of SIN3A-HDAC components and increased levels of acetylated H3 and H4. Interestingly, the ubiquitylation function of CRL4B is not required for the stable retention of SIN3A-HDAC on the promoters of target genes. Thus, in addition to directly contributing to epigenetic silencing by catalyzing H2AK119 monoubiquitylation, CRL4B also facilitates the deacetylation function of SIN3A-HDAC. Our findings reveal a coordinated action between CRL4B and SIN3A-HDAC complexes in transcriptional repression.

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