64
tumor thereby allowing for rapid growth. Sargassum fusiforme polysaccharides
(SFPS) are documented to have an effect on inhibiting the proliferation of
tumor vascular endothelial cells, and its mechanism has to do with downregulating the manifestation of VEGF-A and VEGFR2 in tumor vascular cells
(Chen et al. 2017).
(d) Affecting the signaling pathway of tumor cells. A variety of extracellular and
intracellular signals play an important role in tumor cell apoptosis. Such signals
include tyrosine protein kinase (TPK), cyclic adenosine monophosphate
(cAMP), phosphatidylinositol (PI), nitric oxide (NO), nitric oxide synthase
(NOS), and many others. Epidermal growth factor receptor (EGFR) is similar
to receptor tyrosine kinase (RTK), which is responsible for regulating cell proliferation. The classical pathway of EGFR is Erk (extracellular signal-regulated
enzyme) pathway, which inhibits MT-1 human malignant breast cancer cells
growth, reduces Erk expression and inhibits proliferation of tumor cells through
the Erk signaling pathway (Zhao et al. 2010).
(e) Changes to the biochemical properties of tumor cell membranes. Cell membrane growth characteristics have a lot of influence on the adhesion of the tumor
membrane proteins and tumor cells. The biochemical properties of any cell
membrane are essential to maintain the normal physiological activity and function of cells. Changes in the content of phospholipid membrane sialic acid conversion can kill the tumor cells. Therefore, a decrease in the sialic acid content
will affect the tumor metastasis, antigen exposure associated with the tumor,
immune response cell activation, etc. Phospholipids are converted to phosphatidylinositol phosphate by their enzymatic enzymes, which are involved in the
activation of oncogenes and induction of tumors (Chen et al. 2014; Zhao et al.
2010).
(f) Affecting oncogene. Oncogenes are activated through established chromosomal
alterations such as gene fusion, focal amplification, and translocation
(Hnisz et al. 2016). The study of oncogenes and tumor suppressor genes has
provided strong evidence and targets for elucidating the mechanism of cancer
and the development of gene therapy and antineoplastic drugs. Genes involved
in antitumor effects include the Bcl-2 family, p53 family, C-myc, and so on
(Chen and Huang 2018; Levine and Puzio-Kuter 2010). The anti-apoptotic
genes in Bcl-2 family are Bcl-2, Bcl-xl, Bcl-w, Mcl-1, etc. Apoptotic genes are
Bax, Bak, Bad, Bid, Bim, and so on. p53 is a tumor suppressor gene, c-myc
overexpression will promote tumor cell proliferation. Bcl-2/Bax ratio is also
effective for promoting apoptosis or inhibiting cell apoptosis (Levine and
Puzio-Kuter 2010).
4.7.4.2 Enhancing the Immune Function of Organism
The role which the immune system plays in tumor progression cannot be overemphasized. This is the main reason why tumor immunotherapy is considered as one
of the important treatment strategies for cancer (Carvalho et al. 2016). While some
T. A. Oyedepo and A. A. A. Kayode
tumor thereby allowing for rapid growth. Sargassum fusiforme polysaccharides
(SFPS) are documented to have an effect on inhibiting the proliferation of
tumor vascular endothelial cells, and its mechanism has to do with downregulating the manifestation of VEGF-A and VEGFR2 in tumor vascular cells
(Chen et al. 2017).
(d) Affecting the signaling pathway of tumor cells. A variety of extracellular and
intracellular signals play an important role in tumor cell apoptosis. Such signals
include tyrosine protein kinase (TPK), cyclic adenosine monophosphate
(cAMP), phosphatidylinositol (PI), nitric oxide (NO), nitric oxide synthase
(NOS), and many others. Epidermal growth factor receptor (EGFR) is similar
to receptor tyrosine kinase (RTK), which is responsible for regulating cell proliferation. The classical pathway of EGFR is Erk (extracellular signal-regulated
enzyme) pathway, which inhibits MT-1 human malignant breast cancer cells
growth, reduces Erk expression and inhibits proliferation of tumor cells through
the Erk signaling pathway (Zhao et al. 2010).
(e) Changes to the biochemical properties of tumor cell membranes. Cell membrane growth characteristics have a lot of influence on the adhesion of the tumor
membrane proteins and tumor cells. The biochemical properties of any cell
membrane are essential to maintain the normal physiological activity and function of cells. Changes in the content of phospholipid membrane sialic acid conversion can kill the tumor cells. Therefore, a decrease in the sialic acid content
will affect the tumor metastasis, antigen exposure associated with the tumor,
immune response cell activation, etc. Phospholipids are converted to phosphatidylinositol phosphate by their enzymatic enzymes, which are involved in the
activation of oncogenes and induction of tumors (Chen et al. 2014; Zhao et al.
2010).
(f) Affecting oncogene. Oncogenes are activated through established chromosomal
alterations such as gene fusion, focal amplification, and translocation
(Hnisz et al. 2016). The study of oncogenes and tumor suppressor genes has
provided strong evidence and targets for elucidating the mechanism of cancer
and the development of gene therapy and antineoplastic drugs. Genes involved
in antitumor effects include the Bcl-2 family, p53 family, C-myc, and so on
(Chen and Huang 2018; Levine and Puzio-Kuter 2010). The anti-apoptotic
genes in Bcl-2 family are Bcl-2, Bcl-xl, Bcl-w, Mcl-1, etc. Apoptotic genes are
Bax, Bak, Bad, Bid, Bim, and so on. p53 is a tumor suppressor gene, c-myc
overexpression will promote tumor cell proliferation. Bcl-2/Bax ratio is also
effective for promoting apoptosis or inhibiting cell apoptosis (Levine and
Puzio-Kuter 2010).
4.7.4.2 Enhancing the Immune Function of Organism
The role which the immune system plays in tumor progression cannot be overemphasized. This is the main reason why tumor immunotherapy is considered as one
of the important treatment strategies for cancer (Carvalho et al. 2016). While some
T. A. Oyedepo and A. A. A. Kayode