A person answered these questions from the article, he answered one of them wrong, I want you to find a wrong part and answer why is it wrong?
I put the link for article down below.
Answers based of article:
1. What two main points did you understand from the abstract?
a. In this paper the author wanted to look at the DNA recombinational repairs in CT (cancer/testes) and in lung adenocarcinoma cells. One of the two main points of the abstract of the paper is the of the HORMAD1 germ. It is a germ that is cell restricted and plays a role in the breaking of next-generation breakage in DNA double-strand breaks. The second main point in the abstract was the HORMAD1 gene for this study was used as well for the potential role in genome maintenance in the lung adenocarcinoma cells. Overall, in this abstract, the author wanted to identify the HORMAD1 dependent as a new mechanism for radio-resistance in lung adenocarcinoma cells.
2 2. What methods were used to conduct the research? Why were they appropriate?
a. There several methods used to conduct their research. They were effective and relevant to the research. One of the methods that they used was cell culture and transfection. They looked at the expression of plasmids, and the adenovirus construction and infection. Another important method that was used was RNA interference. Cell culture and transfection are important to keep cell growth and all cells to be healthy. The expressions of each HORMAD1 plasmid were to look at the mutants that were harboring deletions. The adenovirus was to purify the HI1229 and the HORMAD1. The RNA interference was to look at controlled non siRNA and HORMAD1.
3. What key findings did you see in the results?
a. The key finding results are in figure 2. They look at the different functional domains of HORMAD1 on DNA damaged responses. Figure 2a was to study the disordered profile of HORMAD1. In figure 2b it was the infected HI299 cells that were infected with the adenovirus. The key finding that they found was the immunoblot showed a relative expression of the wildtype and mutant forms of HORMAD1. Figure 2c was the same as 2b except for the cells that were infected with the adenovirus vectors encoding with the HA epitope-tagged wild type. The key results indicated that that the HORMA domain and the C-terminal acids of HORMAD1 is necessary for containing the IRIF. The last two figures showed the transfected cells and resulted in anti MYC antibodies.
4. 4. Provide a summary of the authors conclusions.
a. The authors’ conclusions in their paper is that the role of the HORMAD1 in promoting the DSB can repair cancer cells. This also gave another explanation from another study from Wang showing that the HORMAD1 does promote a resistance to PARP inhibitors in breast cancer. With their findings, they found that HORMAD1 inhibits HR in breast cancer. They also concluded that HORMAD1 stimulates HR and also inhibits HR in different settings. An example that used was that a tissue that expresses an HR pathway that is targeted by HORMAD1 can stimulate the HR in lung and in breast cancer but inhibits the HR in the TNBC. Overall, they found that HORMAD1 promotes HR.
5. 5. Were the conclusions accurate for the results presented in the paper?
No, their conclusions were not accurate to their findings of the paper. I believe the author was hoping to have the same explanation as Wangs experiments. What Walkins discovered was that the HORMAD1 gene was expressed with triple-negative breast cancers. They also discovered the same correlation as well with lung adenocarcinoma. Overall they were unable to determine the phenotypic, deficiency, and cell lines of HORMAD1. Though they were able to understand the mechanisms and expression levels of tumor growth within the gene induced in HR cancer cells. This was also a hopeful new approach to look at this specific gene and a way to enhance radiotherapy and a way to possibly kill cancer cells and growth.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192992/pdf/41598_2018_Article_33601.pdf
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