Mitochondrial Dynamics Related Genes -MFN1, MFN2 and DRP1 Polymorphisms are Associated with Risk of Lung Cancer

Liang, Xiaohua; Dang, Shengqiang

doi:10.2147/pgpm.s314860

Cited by 7 publications

(6 citation statements)

References 36 publications

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“…A recent study identified rs879255685 and rs879255689, resulting in DRP1 missense variants G362D and G379K, in lung cancer patient cells. 98 These mutations were earlier reported to be associated with developmental delay, refractory epilepsy, and altered function of peroxisomes and mitochondria. Among the two, DRP1 rs879255689 was reported to be associated with an increased risk of developing lung cancer.…”

Section: Drp1: Snps and Mutationsmentioning

confidence: 96%

“…These mutations were earlier reported to be associated with developmental delay, refractory epilepsy, and altered function of peroxisomes and mitochondria. Among the two, DRP1 rs879255689 was reported to be associated with an increased risk of developing lung cancer …”

Section: Crosstalk Between Drp1 and Cancermentioning

confidence: 99%

“…Among the two, DRP1 rs879255689 was reported to be associated with an increased risk of developing lung cancer. 98 5.2. DRP1: Association with the Various Metabolic Pathways Leading to Cancer.…”

Section: Drp1: Snps and Mutationsmentioning

confidence: 99%

“…Single nucleotide polymorphisms (SNPs) are reported in the DRP1 alleles and are linked to defects that may be lethal (single nucleotide polymorphism database ()). A recent study identified rs879255685 and rs879255689, resulting in DRP1 missense variants G362D and G379K, in lung cancer patient cells . These mutations were earlier reported to be associated with developmental delay, refractory epilepsy, and altered function of peroxisomes and mitochondria.…”

Section: Crosstalk Between Drp1 and Cancermentioning

confidence: 99%

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DRP1: At the Crossroads of Dysregulated Mitochondrial Dynamics and Altered Cell Signaling in Cancer Cells

Adhikary,

Mukherjee,

Banerjee

et al. 2023

ACS Omega

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In the past decade, compelling evidence has accumulated that highlights the role of various subcellular structures in human disease conditions. Dysregulation of these structures greatly impacts cellular function and, thereby, disease conditions. One such organelle extensively studied for its role in several human diseases, especially cancer, is the mitochondrion. DRP1 is a GTPase that is considered the master regulator of mitochondrial fission and thereby also affects the proper functioning of the organelle. Altered signaling pathways are a distinguished characteristic of cancer cells. In this review, we aim to summarize our current understanding of the interesting crosstalk between the mitochondrial structure−function maintained by DRP1 and the signaling pathways that are affected in cancer cells. We highlight the structural aspects of DRP1, its regulation by various modifications, and the association of the protein with various cellular pathways altered in cancer. A better understanding of this association may help in identifying potential pharmacological targets for novel therapies in cancer.

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Section: Drp1: Snps and Mutationsmentioning

confidence: 96%

Section: Crosstalk Between Drp1 and Cancermentioning

confidence: 99%

Section: Drp1: Snps and Mutationsmentioning

confidence: 99%

Section: Crosstalk Between Drp1 and Cancermentioning

confidence: 99%

See 2 more Smart Citations

DRP1: At the Crossroads of Dysregulated Mitochondrial Dynamics and Altered Cell Signaling in Cancer Cells

Adhikary,

Mukherjee,

Banerjee

et al. 2023

ACS Omega

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“…Previous studies have proven that MFN1 and MFN2 are responsible for the fusion and physiological function maintenance of the mitochondria (Liang & Dang, 2021;Yapa et al, 2021). Growing evidences indicate that MFN2 is essential to the maintaining of mammalian follicle development, oocyte maturation, and normal secretion of P4 (Hashem et al, 2020;Zhang et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

MFN2 regulates progesterone biosynthesis and proliferation of granulosa cells during follicle selection in hens

Hou,

Hu,

et al. 2023

Journal Cellular Physiology

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Follicle selection in hens refers to a biological process that only one small yellow follicle (SYF) is selected daily or near‐daily for following hierarchical development (from F5/F6 to F1) until ovulation. MFN2 is a kind of GTPases located on the mitochondrial outer membrane, which plays a crucial role in mitochondrial fusion. This study aimed to elucidate the role of MFN2 in proliferation and progesterone biosynthesis of granulosa cells (GCs) during follicle selection in hens. The results showed that GCs began to produce progesterone (P4) after follicle selection, accompanied with changes from multi‐layer with flat cells to single layer with cubic cells. MFN2 was detected in GCs of follicles from SYF to F1. After follicle selection, the expression level of MFN2 in GCs upregulated significantly, accompanied with increases in P4 biosynthesis, ATP production, mitochondrial DNA (mtDNA) copy numbers of granulosa cells. FSH (80 ng/mL) facilitated the effects of P4 biosynthesis and secretion, ATP production, mtDNA copy numbers, cell proliferation and the MFN2 transcription of granulosa cells from F5 (F5G) in vitro. However, FSH treatment did not promote P4 secretion in granulosa cells from SYF (SYFG) in vitro. Meanwhile, we observed that change fold of MFN2 transcription, ATP production, mtDNA copy numbers and cell proliferation rate in F5G after treatment with FSH were greater than those in SYFG. Furthermore, expression levels of MFN2 protein and messenger RNA in F5G were significantly higher than those in SYFG after treatment with FSH. P4 biosynthesis, ATP production, mtDNA copy numbers as well as cell proliferation reduced significantly in F5G with MFN2 knockdown. Oppositely, P4 biosynthesis, ATP production, mtDNA copy numbers and cell proliferation increased significantly in SYFG after the overexpression of MFN2. Our results suggest that the upregulation of MFN2 may be involved in the initiation of P4 biosynthesis, and promotion of GCs proliferation during follicle selection.

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Mitochondrial dynamics in pulmonary disease: Implications for the potential therapeutics

Li,

Dai,

Zhou

et al. 2024

Journal Cellular Physiology

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Mitochondria are dynamic organelles that continuously undergo fusion/fission to maintain normal cell physiological activities and energy metabolism. When mitochondrial dynamics is unbalanced, mitochondrial homeostasis is broken, thus damaging mitochondrial function. Accumulating evidence demonstrates that impairment in mitochondrial dynamics leads to lung tissue injury and pulmonary disease progression in a variety of disease models, including inflammatory responses, apoptosis, and barrier breakdown, and that the role of mitochondrial dynamics varies among pulmonary diseases. These findings suggest that modulation of mitochondrial dynamics may be considered as a valid therapeutic strategy in pulmonary diseases. In this review, we discuss the current evidence on the role of mitochondrial dynamics in pulmonary diseases, with a particular focus on its underlying mechanisms in the development of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis (PF), pulmonary arterial hypertension (PAH), lung cancer and bronchopulmonary dysplasia (BPD), and outline effective drugs targeting mitochondrial dynamics‐related proteins, highlighting the great potential of targeting mitochondrial dynamics in the treatment of pulmonary disease.

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Mitochondrial Dynamics Related Genes -MFN1, MFN2 and DRP1 Polymorphisms are Associated with Risk of Lung Cancer

Cited by 7 publications

References 36 publications

DRP1: At the Crossroads of Dysregulated Mitochondrial Dynamics and Altered Cell Signaling in Cancer Cells

DRP1: At the Crossroads of Dysregulated Mitochondrial Dynamics and Altered Cell Signaling in Cancer Cells

MFN2 regulates progesterone biosynthesis and proliferation of granulosa cells during follicle selection in hens

Mitochondrial dynamics in pulmonary disease: Implications for the potential therapeutics

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