Cancer is an everyday medical concern which requires an appropriate treatment strategy. The malfunction of cell cycle is a well-established cause for cancer induction. Chemotherapy and radiation are the standard available therapeutic approach for cancer treatment; however severe side effects were reported in association to such treatments, for instance, the efficacy of patients' immune system is adversely affected in apart by radiation. These side effects may be minimized by providing novel remedial preparations. Complementary and alternative medicinal compounds, which were obtained from fresh or marine flora particularly micro and macro algae, were reported to its anti-cancerous activities. Several types of bioactive molecules are also present in microalgae, such as carotenoids, various forms of polysaccharides, vitamins, sterol, fibres, minerals…ect; the great unused biomass of microalgae and their excellent diversity of chemical constituents may introduce a major step in developing of anti-malignant drugs. Previously, such characteristic of microalgal bio-diversity was commercially exploited to make food supplements and gelling substances. However, recently, several investigations were designed to study the potential anti-carcinogenic effect of microalgal extracts, where they mostly concluded their ability to induce apoptotic cancer cell death via caspase dependent or independent pathways. In this review paper, we reported the various species of microalgae that possessed anti-tumor activity, the tumor cell lines altered through using microalgal extracts along with the levels of such extracts that reported to its inhibitor effect against cell cycle and proliferation.

GI24, an immunoglobulin superfamily member, has been cloned from a placenta cDNA library as a gene product that promoted activation of matrix metalloproteinase (MMP)‐2 mediated by membrane type (MT) 1–MMP. Co‐expression of GI24 with MT1‐MMP in HEK293T cells increased the cell‐surface level of MT1‐MMP concomitant with the cleavage of the GI24 at the juxtamembrane site to shed the extracellular domain. HT1080 fibrosarcoma cells stably transfected with the GI24 gene expressed a higher level of MT1‐MMP and showed more invasive ability in collagen gel than the control cells. GI24 was cleaved in HT1080 cells, which was blocked by the administration of MMP inhibitor BB94 or transfection of small interfering RNA (siRNA) targeting MT1‐MMP. GI24 expression is relatively high in some squamous carcinoma and hepatocarcinoma cell lines. Transfection of siRNA for GI24 into oral squamous carcinoma‐derived HSC‐4 cells, which express GI24 and MT1‐MMP genes reduced the expression of not only GI24 but also MT1‐MMP, and attenuated invasive growth in the collagen matrix. These results suggest that GI24 contributes to tumor‐invasive growth in the collagen matrix by augmenting cell surface MT1‐MMP. (Cancer Sci 2010; 101: 2368–2374)

H9N2 avian influenza viruses (AIVs) affect both poultry and humans on a global level, and they are especially prevalent in Egypt. In this study, we sequenced the entire genome of AIV H9N2 isolated from chickens in Egypt in 2021, using next-generation sequencing (NGS) technology. Phylogenetic analysis of the resulting sequences showed that the studied strain was generally monophyletic and grouped within the G1 sublineage of the Eurasian lineage. Four segments (polymerase basic 2 [PB2], polymerase basic 1 [PB1], polymerase acidic [PA], and non-structural [NS]) were related to Egyptian genotype II, while the nucleoprotein (NP), neuraminidase (NA), matrix (M), and haemagglutinin (HA) segments were related to Egyptian genotype I. Molecular analysis revealed that HA protein contained amino acid residues (191H and 234L) that suggested a predilection for attaching to human-like receptors. The antigenic sites of HA had two nonsynonymous mutations: V194I at antigenic site A and M40K at antigenic site B. Furthermore, the R403W and S372A mutations, which have been observed in H3N2 and H2N2 strains that caused human pandemics, were found in the NA protein of the detected strain. The internal proteins contained virulence markers: 504V in the PB2 protein, 622G, 436Y, 207K, and 677T in the PB1 protein, 127V, 550L, and 672L in PA protein, and 64F and 69P in the M protein. These results show that the detected strain had undergone intrasubtype reassortment. Furthermore, it contains changes in the viral proteins that make it more likely to be virulent, raising a question about the tendency of AIV H9N2 to become highly pathogenic in the future for both poultry and humans.

Following ENU mutagenesis, a phenodeviant line was generated, termed the ‘Cartoon mouse’, that exhibits profound defects in growth and development. Cartoon mice harbor a single S466P point mutation in the MT1-MMP hemopexin domain, a 200 amino acid segment that is thought to play a critical role in regulating MT1-MMP collagenolytic activity. Herein, we demonstrate that the MT1-MMP_S466P mutation replicates the phenotypic status of Mt1-mmp-null animals as well as the functional characteristics of MT1-MMP^-/- cells. However, rather than a loss-of-function mutation acquired as a consequence of defects in MT1-MMP proteolytic activity, the S466P substitution generates a misfolded, temperature-sensitive mutant that is abnormally retained in the endoplasmic reticulum (ER). By contrast, the wild-type hemopexin domain does not play a required role in regulating MT1-MMP trafficking as a hemopexin domain-deletion mutant is successfully mobilized to the cell surface and displays near-normal collagenolytic activity. Alternatively, when MT1-MMP_S466P-expresssing cells cultured at a permissive temperature of 25°C that depresses misfolding, the mutant successfully traffics from the ER to the trans-Golgi network (ER→TGN) where it undergoes processing to its mature form, mobilizes to the cell surface and expresses type I collagenolytic activity. Together, these analyses define the Cartoon mouse as an unexpected gain-of-abnormal function mutation wherein the temperature-sensitive mutant phenocopies MT1-MMP^-/- mice as a consequence of eliciting a specific ER→TGN trafficking defect.

Heparanase activity was found to be included in human cancer development and growth. Heparanase (HPSE) gene single nucleotide polymorphisms (SNPs) have been found to be correlated with different human cancers. In the current study, we investigated whether HPSE SNPs were a hepatocellular carcinoma (HCC) risk factor by carrying out a comprehensive case-control pilot study. HPSE rs12331678 and rs12503843 were genotyped in 70 HCC-diagnosed patients and 30 healthy controls by modified amplification refractory mutation system (ARMS PCR) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. HPSE rs12331678 distributions showed that there were no statistically significant differences between both cohorts either in genotypic or allelic distribution but there was a significant correlation between the rs12503843 (T allele) and the HCC risk in the whole samples (P = 0.042). No significant association was observed between the HPSE rs12331678 and rs12503843 gene polymorphisms and all clinicopathologic markers or with SNP stratification based on HCV carrier in HCC groups. Our findings suggest for the first time the HPSE gene SNP characterization in HCC Egyptian patients, and our findings reveal there were associations between the HPSE rs12503843 (T allele) and the susceptibility to HCC.