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Can FASN be used for an anticancer treatment?

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Can FASN be used for an anticancer treatment?

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Since cancer became one of the main causes of death in the world, researchers are fiercely searching for a cure or at least a method to improve the survival time of pacients.

FASN, the schortcut for fatty acid synthase is an enzyme that is catalyzing the synthesis of fatty acids chains in mammals. Also, is a key in maintaining the biological traits of malignant tumor cells (Hess&Igal, 2011). FASN became a target for researchers as a candidate oncogene in different types of cancer, being expressed in high levels in tumors and evidences showed that fatty acid metabolic pathways play a crucial role in carcinogenesis (Yeh et al., 2006).

Sun et al. present us the implication of FASN in cell proliferation, cell migration, in tumor growth and in anoikis (a form of programmed cell death). The researchers performed in vitro studies and then, to confirm their discoveries they carried out studies in vivo on mice with transplanted tumors.

They silenced or overexpressed FASN in different cell lines of osteosarcoma (143B, MG-63, Saos-2) and non-tumor ones (hFOB 1.19) to see the effects. Through different techniques like western blotting, immunofluorescence, qPCR and flow cytometry they observed that the silenced cells showed an inhibited cell migration, invasion and an accelerated death in them, while the overexpression of FASN promoted cell proliferation, cell migration and anoikis was suppressed.

Interestingly, they observed that FASN is exerting its function by regulating the proteins ERK1/2 and Bcl-xL. Upregulation of FASN revealed higher levels of ERK1/2/Bcl-xL while downregulation gave opposite levels of these proteins. They concluded that ERK1/2/Bcl-xL have a role along with FASN in metastasis development.

Drury et al. (focused on colorectal cancer) and Zhang et al. (focused on salivary adenoid cystic carcinoma) support the results of Sun et al. but is still unclear how exactly FASN can induce EMT in cancer cells.

We need to know very well our enemy before we can go to the battle, so every baby-step is extremely important to bring us more closer to the end of this “war on cancer”.

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References:

Drury, J., Rychahou, P. G., He, D., Jafari, N., Wang, C., Lee, E. Y., Weiss, H. L., Evers, B. M., & Zaytseva, Y. Y. (2020). Inhibition of Fatty Acid Synthase Upregulates Expression of CD36 to Sustain Proliferation of Colorectal Cancer Cells. Frontiers in oncology 10, 1185. https://doi.org/10.3389/fonc.2020.01185

Hess, D. & Igal, R. A. (2011). Genistein downregulates de novo lipid synthesis and impairs cell proliferation in human lung cancer cells. Experimental Biology and Medicine (Maywood), 236, (pp. 707–713)

Sun, T., Zhong, X., Song, H., Liu, J., Li, J., Leung, F., Lu,W.W., & Liu, Z. (2019). Anoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma, Cell Death & Disease, volume 10, Article number: 298. https://doi.org/10.1038/s41419-019-1532-2

Zhang, W.,  Wang, S., Jiang, Y., Liu, Y., Yu, X., Wu, J., Wang, K., Pang, X., Liao, P., Liang, X. & Tang, Y. (2020), Fatty acid synthase contributes to epithelial‐mesenchymal transition and invasion of salivary adenoid cystic carcinoma through PRRX1/Wnt/β‐catenin pathway, Journal of Cellular and Molecular medicine 24(19) (pp. 11465-11476), https://doi.org/10.1111/jcmm.15760

Yeh, C.S., Wang, J.Y., Cheng, T.L., Juan, C.H., Wu, C.H., Lin, S.R. (2006). Fatty acid metabolism pathway play an important role in carcinogenesis of human colorectal cancers by Microarray-Bioinformatics analysis. Cancer Letters 233(2), (pp. 297-308). doi: 10.1016/j.canlet.2005.03.050

Fig. A (from Sun et al., 2019) – Effects of FASN silencing and overexpression      on p-ERK1/2 and Bcl-xL in different cell lines

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This is a good study to blog about. Try to make your title accessible and enticing to readers who might not be virologists. You want to make them care enough to read the topic. Make sure your sentences make sense - these sentences don't really make sense "The KoRV is associated with developing diseases such as lymphoid neoplasia, oxalate nephrosis or caused by opportunistic pathogens like Chlamydia pecorum all of them being a major threat for koalas life. " "This study (Sarker et al., 2020) discusses about how important is the level of completeness of KoRV genome in the severity of the disease, to observe the differences between proviral (DNA) and viral (RNA) loads in two populations of koala and to make connections between all of these." They are too long and deal with more than one idea/concept. Keep your sentences focussed and clear. Avoid redundancies like "discusses about". do you htink another source of differences between the two studies might be the timing of sampling? It is not clear what your conlcuding sentence means.

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KoRV, Proviral and Viral loads in two populations of Koalas

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KoRV, Proviral and Viral loads in two populations of Koalas

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Koala retrovirus (KoRV) induce immunodeficiency and tumors. The KoRV is associated with developing diseases such as lymphoid neoplasia, oxalate nephrosis or caused by opportunistic pathogens like Chlamydia pecorum all of them being a major threat for koalas life.

This study (Sarker et al., 2020) discusses about how important is the level of completeness of KoRV genome in the severity of the disease, to observe the differences between proviral (DNA) and viral (RNA) loads in two populations of koala and to make connections between all of these. They used the PCR technique to analyse the presence of particular genes (pol, env and gag genes) in a number of 105 koalas from the southern and 71 koalas from the northern population in Australia males and females, between 2014 to 2017.

It was revealed that koalas from the northern population presented a higher incidence of neoplasia and chlamydiosis (with 100% proviral and viral positive) than koalas from the south but none of the animals from the northern part had oxalate nephrosis. 99% of koalas from the south presented proviral DNA but not all the representative genes and 51,2% were viral RNA positive. Were suggested a number of possible explanations for the variation in viral loads in both populations (mutations, genetic segregation between them). It was observed that animals that did not have all proviral genes were less likely to possess viral RNA or to develop KoRV disease.

However, is important to say that in this study and in similar ones that were performed in the same location were reported different results (Legione et al., 2017). An explanation for the discrepancy in the results may be the health conditions and the origin of studied animals. In this study the animals were rescued because of health conditions while in other studies the animals were from the wild and mostly healthy.

There are a lot more things to know about this devastating virus and scientists make huge efforts to find a solution. Progresses will be made in this direction but at the same time I think the evolution forces are not going to wait.

References:

Legione, A.R., Patterson, J.L., Whiteley, P., Firestone, S.M., Curnick, M., Bodley, K., Lynch, M., Gilkerson, J.R., Sansom, F.M., Devlin, J.M. (2017) Koala retrovirus genotyping analyses reveal a low prevalence of KoRV-A in Victorian koalas and an association with clinical disease. Journal of Medical Microbiology 66, 236–244. doi: https://doi.org/10.1099/jmm.0.000416

Sarker, N., Fabijan, J., Owen, H., Seddon, J., Simmons, G., Speight, N., Kaler, J., Woolford, L., Emes, R.D., Hemmatzadeh, F., Trott, D.J, Meers, J. & Tarlinton, R.E. (2020). Koala retrovirus viral load and disease burden in distinct northern and southern koala populations. Scientific reports 10, Article 263(2020). doi: https://doi.org/10.1038/s41598-019-56546-0