Comparative mitochondrial proteomic analysis of hepatocellular carcinoma from patients

Ye, Yunbin; Huang, Aimin; Huang, Chuanbing; Liu, Jingfeng; Wang, Bin; Lin, Kan; Chen, Qiang; Zeng, Yongyi; Hui-jing, Chen; Tao, Xuan; Wei, Guangya; Wu, Yanbin

doi:10.1002/prca.201100103

Cited by 26 publications

(22 citation statements)

References 37 publications

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“…Several observations indicate that mtSSB is associated with human cancers. For example, the expression level of mtSSB is increased in hepatocellular carcinoma or osteosarcoma tissues when compared to nontumor samples . Very recently, Jiang et al .…”

Section: Introductionmentioning

confidence: 99%

Upregulation of mtSSB by interleukin‐6 promotes cell growth through mitochondrial biogenesis‐mediated telomerase activation in colorectal cancer

Wang

Huang

et al. 2018

Intl Journal of Cancer

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It is now widely accepted that mitochondrial biogenesis is inhibited in most cancer cells. Interestingly, one of the possible exceptions is colorectal cancer (CRC), in which the content of mitochondria has been found to be higher than in normal colon mucosa. However, to date, the causes and effects of this phenomenon are still unclear. In the present study, we systematically investigated the functional role of mitochondrial single‐strand DNA binding protein (mtSSB), a key molecule in the regulation of mitochondrial DNA (mtDNA) replication, in the mitochondrial biogenesis and CRC cell growth. Our results demonstrated that mtSSB was frequently upregulated in CRC tissues and that upregulated mtSSB was associated with poor prognosis in CRC patients. Furthermore, overexpression of mtSSB promoted CRC cell growth in vitro by regulating cell proliferation. The in vivo assay confirmed these results, indicating that the forced expression of mtSSB significantly increases the growth capacity of xenograft tumors. Mechanistically, the survival advantage conferred by mtSSB was primarily caused by increased mitochondrial biogenesis and subsequent ROS production, which induced telomerase reverse transcriptase (TERT) expression and telomere elongation via Akt/mTOR pathway in CRC cells. In addition, FOXP1, a member of the forkhead box family, was identified as a new transcription factor for mtSSB. Moreover, our results also demonstrate that proinflammatory IL‐6/STAT3 signaling facilitates mtSSB expression and CRC cell proliferation via inducing FOXP1 expression. Collectively, our findings demonstrate that mtSSB induced by inflammation plays a critical role in the regulation of mitochondrial biogenesis, telomerase activation, and subsequent CRC proliferation, providing a strong evidence for mtSSB as drug target in CRC treatment.

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Section: Introductionmentioning

confidence: 99%

Upregulation of mtSSB by interleukin‐6 promotes cell growth through mitochondrial biogenesis‐mediated telomerase activation in colorectal cancer

Wang

Huang

et al. 2018

Intl Journal of Cancer

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“…Although the molecular mechanisms have gradually been deciphered, the function of mitochondria in the process of lung cancer metastasis remains unknown. Some studies have demonstrated that in certain tumors, such as nasopharyngeal and hepatocellular carcinoma, mitochondrial proteins are the potential biomarkers for cancer initiation and progression . Therefore, we proposed that mitochondrial proteins might be differentially expressed in lung cancer metastasis.…”

Section: Discussionmentioning

confidence: 94%

“…Mitochondria are important organelles in cellular physiology. They have their own genomic system independent from the nucleus, and possess their own transcription, translation, and protein assembly machinery . They are the principal suppliers of adenosine triphosphate, playing a central role in cellular energy metabolism and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Comparative mitochondrial proteomic analysis of human large cell lung cancer cell lines with different metastasis potential

Liu

et al. 2019

Thoracic Cancer

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Background Lung cancer is a highly aggressive cancer with a poor prognosis and is associated with distant metastasis; however, there are no clinically recognized biomarkers for the early diagnosis and prediction of lung cancer metastasis. We sought to identify the differential mitochondrial protein profiles and understand the molecular mechanisms governing lung cancer metastasis. Methods Mitochondrial proteomic analysis was performed to screen and identify the differential mitochondrial protein profiles between human large cell lung cancer cell lines with high (L‐9981) and low (NL‐9980) metastatic potential by two‐dimensional differential gel electrophoresis. Western blot was used to validate the differential mitochondrial proteins from the two cells. Bioinformatic proteome analysis was performed using the Mascot search engine and messenger RNA expression of the 37 genes of the differential mitochondrial proteins were detected by real‐time PCR. Results Two hundred and seventeen mitochondrial proteins were differentially expressed between L‐9981 and NL‐9980 cells ( P < 0.05). Sixty‐four analyzed proteins were identified by matrix‐assisted laser desorption/ionization‐time of flight mass spectrometry coupled with database interrogation. Ontology analysis revealed that these proteins were mainly involved in the regulation of translation, amino acid metabolism, tricarboxylic acid cycle, cancer invasion and metastasis, oxidative phosphorylation, intracellular signaling pathway, cell cycle, and apoptosis. Conclusion Our results suggest that the incorporation of more samples and new datasets will permit the definition of a collection of proteins as potential biomarkers for the prediction and diagnosis of lung cancer metastasis.

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“…PEBP1 maybe one of the first anti-oncogenes to be downregulated, which may be one of the factors that facilitates the invasion and metastasis of tumor cells after IR injury. We comparatively analyzed the mitochondrial proteins in HCC and non-cancerous tissues by two-dimensional gel electrophoresis, which revealed that the expression of PEBP1 was significantly lower in cancer tissues [20]. Therefore, a drug targeted to PEBP1 may be useful to reduce the recurrence and metastasis of liver cancer after surgery.…”

Section: Discussionmentioning

confidence: 99%

Somatostatin Octapeptide Inhibits Cell Invasion and Metastasis in Hepatocellular Carcinoma Through PEBP1

Huang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatocellular carcinoma (HCC) is a major threat to human health. The condition carries a high risk of death; 45% of new cases occur in China. Surgical resection is the first choice for treatment of HCC, but 30.9% of patients experience recurrence within 6 months after the operation. To improve patient survival, we must determine how to reduce the probability of recurrence and metastasis and elucidate the underlying mechanism of disease. We therefore studied the effect of somatostatin octapeptide (octreotide) on the invasion and metastasis of HCC. Methods: The migration and invasion cytological tests were used to detect the effect of octreotide on liver cancer cells (SK-Hep-1 and HepG2). PEBP1 RNAi was used to knockdown expression. Invasion and metastasis were measured with transwell migration and wound-healing assays. Western blotting was used to detect changes in levels of PEBP1 and invasion pathway proteins after octreotide treatment. The effect of octreotide was studied in vivo by establishing a pulmonary metastasis model using SK-Hep-1 cells in nude mice. In-vivo bioluminescence imaging and hematoxylin and eosin staining of lung tissue were used to verify the results. Results: Increasing concentrations of octreotide were progressively more effective in halting the invasion and metastasis of liver cancer cells. Octreotide may upregulate PEBP1, TIMP-2, and E-cadherin while downregulating MMP-2 and Twist to inhibit cell invasion and metastasis. And downregulation of PEBP1 would also change the expression of MMP-2, TIMP-2 and Twist. The in-vivo experiments showed no cancer cell metastasis in 4 of the 6 mice in the octreotide-treatment group, while all of the mice in the control group displayed pulmonary metastasis of human HCC cells. And the survival period of the mice in the octreotide-treatment group was significantly prolonged. Conclusions: Octreotide may weaken invasion and metastasis through the upregulation of PEBP1. Octreotide may reduce the risk of recurrence and metastasis after surgery for liver cancer.

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Comparative mitochondrial proteomic analysis of hepatocellular carcinoma from patients

Cited by 26 publications

References 37 publications

Upregulation of mtSSB by interleukin‐6 promotes cell growth through mitochondrial biogenesis‐mediated telomerase activation in colorectal cancer

Upregulation of mtSSB by interleukin‐6 promotes cell growth through mitochondrial biogenesis‐mediated telomerase activation in colorectal cancer

Comparative mitochondrial proteomic analysis of human large cell lung cancer cell lines with different metastasis potential

Somatostatin Octapeptide Inhibits Cell Invasion and Metastasis in Hepatocellular Carcinoma Through PEBP1

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