Correction: Mitochondrial DNA variation in Alzheimer’s disease reveals a unique microprotein called SHMOOSE

Miller, Brendan; Kim, Su-Jeong; Mehta, Hemal H.; Cao, Kevin; Kumagai, Hiroshi; Thumaty, Neehar; Leelaprachakul, Naphada; Braniff, Regina Gonzalez; Jiao, Henry; Vaughan, Joan; Diedrich, Jolene K.; Saghatelian, Alan; Arpawong, Thalida Em; Crimmins, Eileen M.; Ertekin-Taner, Nilüfer; Tubi, Meral A.; Hare, Evan T.; Braskie, Meredith N.; Décarie-Spain, Léa; Kanoski, Scott E.; Grodstein, Francine; Bennett, David A.; Zhao, Lu; Toga, Arthur W.; Wan, Junxiang; Yen, Kelvin; Cohen, Pinchas

doi:10.1038/s41380-023-01956-w

Cited by 6 publications

(2 citation statements)

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“… 22 . Additionally, IMMT regulates the biological behavior of tumor cells by modulating the dynamic processes of mitochondrion division, fusion, transportation, degradation, and biogenesis 23 , 24 . Therefore, this study further investigated the function of IMMT using in vitro experiments.…”

Section: Discussionmentioning

confidence: 99%

Suppressing mitochondrial inner membrane protein (IMMT) inhibits the proliferation of breast cancer cells through mitochondrial remodeling and metabolic regulation

Liu,

Zhao,

Xiong

et al. 2024

Sci Rep

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Metabolic reprogramming is widely recognized as a hallmark of malignant tumors, and the targeting of metabolism has emerged as an appealing approach for cancer treatment. Mitochondria, as pivotal organelles, play a crucial role in the metabolic regulation of tumor cells, and their morphological and functional alterations are intricately linked to the biological characteristics of tumors. As a key regulatory subunit of mitochondria, mitochondrial inner membrane protein (IMMT), plays a vital role in degenerative diseases, but its role in tumor is almost unknown. The objective of this research was to investigate the roles that IMMT play in the development and progression of breast cancer (BC), as well as to elucidate the underlying biological mechanisms that drive these effects. In this study, it was confirmed that the expression of IMMT in BC tissues was significantly higher than that in normal tissues. The analysis of The Cancer Genome Atlas (TCGA) database revealed that IMMT can serve as an independent prognostic factor for BC patients. Additionally, verification in clinical specimens of BC demonstrated a positive association between high IMMT expression and larger tumor size (> 2 cm), Ki-67 expression (> 15%), and HER-2 status. Furthermore, in vitro experiments have substantiated that the suppression of IMMT expression resulted in a reduction in cell proliferation and alterations in mitochondrial cristae, concomitant with the liberation of cytochrome c, but it did not elicit mitochondrial apoptosis. Through Gene Set Enrichment Analysis (GSEA) analysis, we have predicted the associated metabolic genes and discovered that IMMT potentially modulates the advancement of BC through its interaction with 16 metabolic-related genes, and the changes in glycolysis related pathways have been validated in BC cell lines after IMMT inhibition. Consequently, this investigation furnishes compelling evidence supporting the classification of IMMT as prognostic marker in BC, and underscoring its prospective utility as a novel target for metabolic therapy.

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Section: Discussionmentioning

confidence: 99%

Suppressing mitochondrial inner membrane protein (IMMT) inhibits the proliferation of breast cancer cells through mitochondrial remodeling and metabolic regulation

Liu,

Zhao,

Xiong

et al. 2024

Sci Rep

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“…To date, evidence of the mitochondrial role as an initiator of AD is emerging. Multiple heteroplasmic mitochondrial DNA (mtDNA) mutations have been reported in AD patients [ 85 – 89 ]. Previous studies have shown that transferring platelet mtDNA from AD patients into cells with depletion of endogenous mtDNA promotes AD-like changes [ 90 , 91 ], these findings as well as the association of mtDNA haplogroups with AD risk [ 92 ] add credit to the hypothesis of mitochondria-related mode of transmission in the development of this neurodegenerative disorder.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer’s disease

Tian,

Jia,

Wang

et al. 2024

Transl Psychiatry

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The etiopathogenesis of late-onset Alzheimer’s disease (AD) is increasingly recognized as the result of the combination of the aging process, toxic proteins, brain dysmetabolism, and genetic risks. Although the role of mitochondrial dysfunction in the pathogenesis of AD has been well-appreciated, the interaction between mitochondrial function and genetic variability in promoting dementia is still poorly understood. In this study, by tissue-specific transcriptome-wide association study (TWAS) and further meta-analysis, we examined the genetic association between mitochondrial solute carrier family (SLC25) genes and AD in three independent cohorts and identified three AD-susceptibility genes, including SLC25A10, SLC25A17, and SLC25A22. Integrative analysis using neuroimaging data and hippocampal TWAS-predicted gene expression of the three susceptibility genes showed an inverse correlation of SLC25A22 with hippocampal atrophy rate in AD patients, which outweighed the impacts of sex, age, and apolipoprotein E4 (ApoE4). Furthermore, SLC25A22 downregulation demonstrated an association with AD onset, as compared with the other two transcriptome-wide significant genes. Pathway and network analysis related hippocampal SLC25A22 downregulation to defects in neuronal function and development, echoing the enrichment of SLC25A22 expression in human glutamatergic neurons. The most parsimonious interpretation of the results is that we have identified AD-susceptibility genes in the SLC25 family through the prediction of hippocampal gene expression. Moreover, our findings mechanistically yield insight into the mitochondrial cascade hypothesis of AD and pave the way for the future development of diagnostic tools for the early prevention of AD from a perspective of precision medicine by targeting the mitochondria-related genes.

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An Inner Mitochondrial Membrane Microprotein from the SLC35A4 Upstream ORF Regulates Cellular Metabolism

Rocha,

Pai,

Perkins

et al. 2024

Journal of Molecular Biology

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Correction: Mitochondrial DNA variation in Alzheimer’s disease reveals a unique microprotein called SHMOOSE

Cited by 6 publications

References 0 publications

Suppressing mitochondrial inner membrane protein (IMMT) inhibits the proliferation of breast cancer cells through mitochondrial remodeling and metabolic regulation

Suppressing mitochondrial inner membrane protein (IMMT) inhibits the proliferation of breast cancer cells through mitochondrial remodeling and metabolic regulation

Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer’s disease

An Inner Mitochondrial Membrane Microprotein from the SLC35A4 Upstream ORF Regulates Cellular Metabolism

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