The Entanglement between Mitochondrial DNA and Tumor Metastasis

Wu, Qiwei; Tsai, Hsiang‐i; Zhu, Haitao; Wang, Dongqing

doi:10.3390/cancers14081862

Cited by 9 publications

(3 citation statements)

References 130 publications

(154 reference statements)

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“…Juntermanns et al reported that high-dose of radiation ( 20Gy) can damage the tumor's vascular obviously and induce the hypoxic condition of the tumor microenvironment [48], and then hypoxia inducible factor 1 (HIF-1α) incurred in the hypoxic condition can activate migratory and angiogenic genes such as VEGF, MMP-2, and Vimentin [49][50][51]. Other studies reported that radiation induces tumor metastasis through cytokine/chemokine signaling [52] or mitochondrial damage [53,54].…”

Section: Discussionmentioning

confidence: 99%

Carbon ion irradiation suppresses angiogenic response in human lung adenocarcinoma cells mediated by LINC00167/miR-663a/TGF-β1 axis

Huang¹,

Xu²,

Guo³

et al. 2022

Preprint

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Background Radiotherapy plays an important role in numerous tumor clinical treatments and over 65% of cancer patients need to accept radiotherapy all over the world. However, tumor angiogenesis and metastasis induced by conventional photon radiotherapy adversely impact the survival of patients, and limit the clinical radiotherapy efficiency. Heavy-ion radiotherapy has attracted wide attention in recent years because of its excellent physical property and outstanding tumor control rate, however, the underlying gene expression regulation mechanism response to heavy-ion irradiation remains elusive. Methods RNA-sequencing (RNA-seq) and public database analysis were employed to identify the differential molecular changes in lung adenocarcinoma cells exposed to both X-ray and carbon ion (C-ion) irradiation. The expression of the identified LINC00167 was verified by real-time quantitative PCR in different lung cancer cell lines and pulmonary bronchial epithelial cell lines. The content of serum vascular endothelial growth factor (VEGF) and transforming growth factor beta 1 (TGF-β1) of 8 lung cancer patients who received X-ray or carbon ion radiotherapy were detected by ELISA experiment. Loss-of-function and gain-of-function experiments were performed to explore the biological roles of LINC00167 and miR-663a in lung cancer cell angiogenesis and metastasis. Comprehensive biochemical and biological techniques were utilized to explore the functions of LINC00167 in tumor angiogenesis and metastasis induced by different radiation types. Results In this study, we confirmed that LINC00167 was highly expressed and induced by X-ray irradiation in lung cancer cells. Moreover, increased LINC00167 expression was positively correlated with tumor angiogenesis and metastasis caused by conventional photon radiotherapy. LINC00167 worked as a sponge of miR-663a to positively regulate the expression of TGF-β1 and the downstream VEGF signaling and then promoted the tumor angiogenesis and metastasis of lung cancer cells. LINC00167 could strengthen the pro-angiogenesis and metastasis ability of lung cancer cells. Photon radiation-induced LINC00167 promoted angiogenesis both in vitro and in vivo. Conclusion Our data suggest that LINC00167/miR-663a/TGF-β1 axis is involved in the differential angiogenic response of lung adenocarcinoma cells exposed to X-ray or C-ion irradiation, providing the molecular mechanisms underlying the suppressed angiogenic response induced by carbon ion radiotherapy.

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Section: Discussionmentioning

confidence: 99%

Carbon ion irradiation suppresses angiogenic response in human lung adenocarcinoma cells mediated by LINC00167/miR-663a/TGF-β1 axis

Huang¹,

Xu²,

Guo³

et al. 2022

Preprint

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“…The morphology, localization, and functions of mitochondria in CSCs differ from normal cells, normal stem cells, and cancer cells. [163][164][165][166] CSCs express fewer mitochondrial DNA copies (mtDNA) and low levels of mitochondrial transcription factor A (TFAM) in contrast to normal cells which express many copies of mtDNA and TFAM. 163,165,166 Notably, during the process of fibroblast remodeling into iPSCs, a significant reduction in the number of mitochondria takes place, accompanied by decreased mtDNA, mitochondrial mass, and low ROS levels in the stem cells.…”

Section: Mitochondrion -A Key Organelle In Cancer Stem Cellsmentioning

confidence: 99%

Mitochondria in Cancer Stem Cells: From an Innocent Bystander to a Central Player in Therapy Resistance

Garimella,

Gampa,

Chaturvedi

2023

SCCAA

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Cancer continues to rank among the world’s leading causes of mortality despite advancements in treatment. Cancer stem cells, which can self-renew, are present in low abundance and contribute significantly to tumor recurrence, tumorigenicity, and drug resistance to various therapies. The drug resistance observed in cancer stem cells is attributed to several factors, such as cellular quiescence, dormancy, elevated aldehyde dehydrogenase activity, apoptosis evasion mechanisms, high expression of drug efflux pumps, protective vascular niche, enhanced DNA damage response, scavenging of reactive oxygen species, hypoxic stability, and stemness-related signaling pathways. Multiple studies have shown that mitochondria play a pivotal role in conferring drug resistance to cancer stem cells, through mitochondrial biogenesis, metabolism, and dynamics. A better understanding of how mitochondria contribute to tumorigenesis, heterogeneity, and drug resistance could lead to the development of innovative cancer treatments.

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“…EMT has also been associated with mitochondrial dysfunction, which regulates the tumor microenvironment, leading to more aggressive tumors. Wu and colleagues reviewed the recent progress in the regulation of cancer metastasis by mitochondrial DNA, showing its impact on different aspects, including resistance to anoikis, promotion of angiogenesis, cancer cell survival in the circulatory system, and colonization [10]. Moreover, mitochondrial dysfunction leads to metabolic reprogramming and proteome rewiring.…”

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confidence: 99%