Sepia Ink Oligopeptide Induces Apoptosis of Lung Cancer Cells via Mitochondrial Pathway

Wang, Xiaohua; Chen, Cheng; Zhou, Guoren; Ye, Jinjun; Yin, Rong; Feng, Dan; Zhang, Shuai; Wang, Xiaojun; Zhao, Xin; Zhi, Zhang

doi:10.1159/000488046

Cited by 13 publications

(10 citation statements)

References 31 publications

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“…Interestingly, peptide B11 treatment caused a decrease in antiapoptotic Bcl-2 protein, but an increase in proapototic Bax in HeLa cells (Figure 5C(ii),(iii)). This observation is similar to that previously reported by Wang et al, where an oligopeptide from Sepia ink induced the apoptosis of lung cancer cells via the mitochondrial pathway [57]. The antiapoptotic Bcl-2 family proteins prevent cell death induced by various apoptotic stimuli by inhibiting the release of mitochondrial cytochrome C, and inhibiting the activation of caspase-9 and caspase-3 [58].…”

Section: Discussionsupporting

confidence: 89%

A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells’ Proliferation

et al. 2018

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Antimicrobial peptides play important roles in the immune response to pathogens and tumor cells; for this reason, they are being exploited for therapeutic use. In this study, we describe a Litopenaeus vannamei hemocyanin-derived peptide, denoted B11, which shares similar features with other anticancer peptides and attenuates the proliferation of cancer cells. Cell viability assay revealed that B11 significantly inhibited the proliferation of human cervical (HeLa), human hepatocellular carcinoma (HepG2), and human esophageal cancer (EC109) cancer cell lines, but not normal liver cell lines (T-antigen-immortalized human liver epithelial (THLE) cells or THLE-3), by inducing morphological changes, nuclear condensation, and margination, features which are indicative of apoptosis. Besides, peptide B11-induced apoptosis was confirmed by isothiocyanate-labeled Annexin V/propidium iodide (Annexin V-FITC/PI) double staining of HeLa cells. Moreover, cell uptake studies, confocal microscopy, and Western blot analysis revealed that rhodamine-labeled B11 permeated HeLa cells and localized to the mitochondria, causing mitochondria dysfunction through lost mitochondrial membrane potential, which consequently triggered the induction of apoptosis. Increased expression levels of caspase-9, caspase-3, and Bax (Bcl-2-associated X) proteins, coupled with a decrease in Bcl-2 (B-cell lymphoma 2) protein, confirmed that peptide B11 induced apoptosis via the mitochondrial pathway. Thus, the hemocyanin-derived peptide, B11, inhibits the proliferation of cancer cells by causing mitochondrial dysfunction and inducing apoptotic cell death, for which reason it could be explored as an anticancer peptide.

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Section: Discussionsupporting

confidence: 89%

A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells’ Proliferation

et al. 2018

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“…Mitochondria are ubiquitous cellular organelles that are responsible for energy metabolism in eukaryotic cells and have been associated with various conditions, including Alzheimer's disease, Parkinson's disease, diabetes mellitus, various cardiovascular diseases, and lung cancer . Mitochondrial DNA mutations and associated disorders are also related to tumor development, growth, angiogenesis, and metastasis .…”

Section: Introductionmentioning

confidence: 99%

Quantitative proteomic analysis of mitochondrial proteins differentially expressed between small cell lung cancer cells and normal human bronchial epithelial cells

Zhang

Deng

et al. 2018

Thoracic Cancer

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BackgroundSmall cell lung cancer (SCLC) is highly aggressive and is associated with a dismal prognosis. However, there are no clinically recognized biomarkers for early diagnosis. In this study, we used quantitative proteomics to build differential mitochondrial protein profiles that may be used for early diagnosis and investigated the pathogenesis of lung cancer.MethodsWe cultured SCLC cells (NCI‐H446) and normal human bronchial epithelial cells (16‐HBE); mitochondria were extracted and purified using differential and Percoll density gradient centrifugation. Subsequently, we used Western blot analysis to validate mitochondrial purity and labeled proteins/peptides from NCI‐H446 and 16‐HBE cells using relative and absolute quantification of ectopic tags. We then analyzed mixed samples and identified proteins using two‐dimensional liquid chromatography‐tandem mass spectrometry. Additionally, we performed subsequent bioinformatic proteome analyses using the programs ExPASy, GOA, and STRING. Finally, the relationship between ornithine aminotransferase expression and clinicopathological features in lung cancer patients was evaluated using immunohistochemistry.ResultsOne hundred and fifty‐three mitochondrial proteins were differentially expressed between 16‐HBE and NCI‐H446 cells. The expression of 30 proteins between 16‐HBE and NCI‐H446 cells increased more than 1.3‐fold. The upregulation of ornithine aminotransferase was associated with pathological grade and clinical tumor node metastasis stage.ConclusionOur experiment represented a promising method for building differential mitochondrial protein profiles between NCI‐H446 and 16‐HBE cells. Such analysis may also help to identify novel biomarkers of lung cancer.

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“…The expression of calpain-2 was significantly upregulated when TM induced ERS in human breast cancer cells (Han et al, 2015). Studies have shown that blocking the ERS pathway by ALLN pretreatment can significantly prolong the survival rate of liver cancer cells (Wang et al, 2018a). In this study, immunocytochemical staining results showed that calpain-2 was expressed in the cytoplasm of HSC.…”

Section: Discussionmentioning

confidence: 49%

Tunicamycin Induces Hepatic Stellate Cell Apoptosis Through Calpain-2/Ca2 +-Dependent Endoplasmic Reticulum Stress Pathway

Liu

Dai

Wang

et al. 2021

Front. Cell Dev. Biol.

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It has been reported that calpain/caspase-mediated apoptosis induced by endoplasmic reticulum stress (ERS) in hepatic stellate cells (HSCs) by previous studies. At present, the activation of HSC is an important cause of liver fibrosis, and the induction of HSC apoptosis plays an irreplaceable role in reversing liver fibrosis. Therefore, it is of great significance to explore mechanisms of action that can induce HSC apoptosis for the reversal of hepatic fibrosis and the clinical prevention and treatment of hepatic-fibrosis-related diseases such as hepatitis, cirrhosis, and liver cancer. In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2. Our findings indicate that tunicamycin can induce HSCs apoptosis through calpain-2/Ca2+-dependent ERS pathway.

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Sepia Ink Oligopeptide Induces Apoptosis of Lung Cancer Cells via Mitochondrial Pathway

Cited by 13 publications

References 31 publications

A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells’ Proliferation

A Litopenaeus vannamei Hemocyanin-Derived Antimicrobial Peptide (Peptide B11) Attenuates Cancer Cells’ Proliferation

Quantitative proteomic analysis of mitochondrial proteins differentially expressed between small cell lung cancer cells and normal human bronchial epithelial cells

Tunicamycin Induces Hepatic Stellate Cell Apoptosis Through Calpain-2/Ca2 +-Dependent Endoplasmic Reticulum Stress Pathway

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