Loss of the dermis zinc transporter ZIP13 promotes the mildness of fibrosarcoma by inhibiting autophagy

Lee, Mi-Gi; Choi, Mona; Chae, Sehyun; Kang, Mi Young; Jo, Hantae; Baek, Jin-myoung; In, Kyu-Ree; Park, Hyein; Heo, Hyojin; Jang, Dongmin; Brito, Sofia; Kim, Sung Tae; Kim, Dae-Ok; Lee, Jong-Soo; Kim, Jae-Ryong; Bin, Bum-Ho

doi:10.1038/s41598-019-51438-9

Cited by 10 publications

(4 citation statements)

References 48 publications

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“…Previous studies have reported that changes in zinc transport proteins were associated with the occurrence of autophagy [ 44 ]. Knockdown of Zip13 in fibroblasts reduced the expression of LC3-I/II and caused severe autophagy defects [ 45 ]. Moreover, inhibition of Zip1 induced mitophagy by reducing mitochondrial membrane potential, suggesting that Zinc transport proteins play crucial roles in regulating autophagy [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Liu,

Li,

Lan

et al. 2024

J Ovarian Res

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Zinc (Zn) is a crucial trace element essential for human growth and development, particularly for reproductive health. Previous research has shown a decrease in serum zinc concentration with age and individuals with conditions such as polycystic ovary syndrome (PCOS) and diabetes mellitus. However, the specific effects of zinc deficiency on the female reproductive system, especially ovarian function, are not fully understood. In our study, we observed a significant reduction in the total number of follicles and mature follicles in the zinc deficiency group. This reduction correlated with decreased level of anti-Mullerian hormone (AMH) and abnormal gene expression affecting hormone secretion regulation. Furthermore, we found that zinc deficiency disrupted mitochondrial dynamics, leading to oxidative stress in the ovaries, which further inhibited autophagy and increased ovarian apoptosis. These changes ultimately resulted in the failure of germinal vesicle breakdown (GVBD) and reduced oocyte quality. Meanwhile, administration of zinc glycine effectively alleviated the oocyte meiotic arrest caused by dietary zinc deficiency. In conclusion, our findings demonstrated that dietary zinc deficiency can affect hormone secretion and follicle maturation by impairing mitochondrial function and autophagy.

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Section: Discussionmentioning

confidence: 99%

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Liu,

Li,

Lan

et al. 2024

J Ovarian Res

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“…In turn, proteasome inhibitors combined with the inhibition of autophagy induced more human prostate cancer cell death [ 27 ]. The inhibition of autophagy by TPEN (that also chelates zinc) positively affected fibrosarcoma by killing cancer cells selectively [ 28 ]. Similar trends were obtained in our study when HT-1080 cells were cotreated with the compound and CQ, and the decline in cell viability was more significant than in the presence of the compound alone.…”

Section: Discussionmentioning

confidence: 99%

Studies on Autophagy and Apoptosis of Fibrosarcoma HT-1080 Cells Mediated by Chalcone with Indole Moiety

Honkisz-Orzechowska,

Barczyk-Woźnicka,

Kaleta

et al. 2024

IJMS

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This study demonstrated the anticancer efficacy of chalcones with indole moiety (MIPP, MOMIPP) in fibrosarcoma cells for the first time. The results showed that MIPP and MOMIPP reduced the viability of HT-1080 cells in a concentration-dependent manner. MOMIPP was more active than MIPP in HT-1080 cells, showing lower IC50 values (3.67 vs. 29.90 μM). Both compounds at a concentration of 1 μM induced apoptosis in HT-1080 cells, causing death strictly related to caspase activation, as cell viability was restored when the caspase inhibitor Z-VAD was added. Reactive oxygen species production was approximately 3-fold higher than in control cells, and cotreatment with the inhibitor of mitochondrial ATPase oligomycin diminished this effect. Such effects were also reflected in mitochondrial dysfunction, including decreased membrane potential. Interestingly, the compounds that were studied caused massive vacuolization in HT-1080 cells. Immunocytochemical staining and TEM analysis showed that HT-1080 cells exhibited increased expression of the LC3-II protein and the presence of autophagosomes with a double membrane, respectively. Both compounds induced apoptosis, highlighting a promising link between autophagy and apoptosis. This connection could be a new target for therapeutic strategies to overcome chemoresistance, which is a significant cause of treatment failure and tumour recurrence in fibrosarcoma following traditional chemotherapy.

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“…Lee et al investigated the role of the dermis zinc transporter, ZIP13, in fibrosarcoma progression in dermal fibroblasts obtained from wild-type and ZIP13-KO mice [89]. They observed impairment in autophagy in ZIP13 −/− cells associated with low expression of LC3 at the mRNA and protein levels.…”

Section: Zinc and Autophagymentioning

confidence: 99%

Zinc and Autophagy in Age-Related Macular Degeneration

Błasiak

Pawłowska

Chojnacki

et al. 2020

IJMS

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Zinc supplementation is reported to slow down the progression of age-related macular degeneration (AMD), but there is no general consensus on the beneficiary effect on zinc in AMD. As zinc can stimulate autophagy that is declined in AMD, it is rational to assume that it can slow down its progression. As melanosomes are the main reservoir of zinc in the retina, zinc may decrease the number of lipofuscin granules that are substrates for autophagy. The triad zinc–autophagy–AMD could explain some controversies associated with population studies on zinc supplementation in AMD as the effect of zinc on AMD may be modulated by genetic background. This aspect was not determined in many studies regarding zinc in AMD. Zinc deficiency induces several events associated with AMD pathogenesis, including increased oxidative stress, lipid peroxidation and the resulting lipofuscinogenesis. The latter requires autophagy, which is impaired. This is a vicious cycle-like reaction that may contribute to AMD progression. Promising results with zinc deficiency and supplementation in AMD patients and animal models, as well as emerging evidence of the importance of autophagy in AMD, are the rationale for future research on the role of autophagy in the role of zinc supplementation in AMD.

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Loss of the dermis zinc transporter ZIP13 promotes the mildness of fibrosarcoma by inhibiting autophagy

Cited by 10 publications

References 48 publications

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Studies on Autophagy and Apoptosis of Fibrosarcoma HT-1080 Cells Mediated by Chalcone with Indole Moiety

Zinc and Autophagy in Age-Related Macular Degeneration

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