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Evidence based on Mendelian randomization: Causal relationship between mitochondrial biological function and lung cancer and its subtypes.
Zhu et al., Neoplasia 2023
DOI: 10.1016/j.neo.2023.100950
Oh, look at us, we’re so fancy with our big words and complex research methods. We decided to investigate the causal relationship between mitochondrial biological function and lung cancer, including its subtypes, via MR. We used SNPs significantly associated with lung cancer and its subtypes as instrumental variables. Because, you know, why make things simple when you can make them complicated?
We used all sorts of fancy statistical methods like MR-Egger regression, simple mode, weighted mode, simple median, and weighted median. Because, again, why use one method when you can use five?
We found that NADH dehydrogenase (ubiquinone) flavoprotein 2 and transmembrane protein 70 have a causal relationship with lung adenocarcinoma, acting as protective factors. We also found a causal relationship between mitochondrial import inner membrane translocase subunit and NADH dehydrogenase (ubiquinone) iron-sulfur protein 4 and small-cell lung cancer, acting as risk factors. And NADH dehydrogenase (ubiquinone) 1 beta subcomplex subunit 8 was found to have a causal relationship with small-cell lung cancer, acting as a protective factor.
And, just to add a cherry on top, NAD-dependent protein deacylase sirtuin-5 was causally linked to lung squamous cell carcinoma, serving as a protective factor.
We even made a pretty funnel plot to show the symmetrical distribution of the SNPs. And we did a pleiotropy test (P > 0.05) and a “leave-one-out” test to validate the relative stability of the results. Because, you know, we’re thorough like that.
So, in conclusion, we established a causal relationship between mitochondrial biological function and lung cancer, including its subtypes. Aren’t we clever?
