Histidine‐rich calcium binding protein promotes growth of hepatocellular carcinoma <i>in vitro</i> and <i>in vivo</i>

Liu, Jingmei; Han, Ping; Li, Mengke; Yan, Wei; Liu, Jiqiao; He, Jianzhong; Gong, Jin; Wang, Yunwu; Tian, Dean

doi:10.1111/cas.12743

Cited by 19 publications

(21 citation statements)

References 29 publications

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“…Inhibition of ER stress prevented hepatic fibrosis by attenuating HSC activation ( Men et al, 2015 ). Our previous study showed that HRC promoted the growth of liver cancer by inhibiting ER stress-induced apoptosis ( Liu et al, 2015 ). However, the effect of HRC on ER stress in HSCs remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of histidine-rich calcium binding protein (HRC) suppresses liver fibrosis by inhibiting the activation of hepatic stellate cells

Liu

Gong

et al. 2016

Biology Open

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The histidine-rich calcium-binding protein (HRC) is a regulator of Ca2+ homeostasis and it plays a significant role in hepatocellular carcinoma (HCC) progression. However, the relationship between HRC and liver fibrogenesis is still unknown. Our data demonstrates that HRC was upregulated in fibrotic liver and activated hepatic stellate cells (HSCs). TGF-β treatment increased α-SMA and HRC expression dose-dependently in HSCs. Repression of HRC reduced α-SMA, CTGF and collagen expression, and inhibited HSC proliferation and migration. In addition, we found that the anti-fibrosis effect of HRC knockdown was associated with endoplasmic reticulum (ER) stress. Silencing of HRC decreased the expression of ER stress and autophagy markers. Moreover, ER stress agonist thapsigargin (TG) enhanced, whereas ER stress antagonist 4-phenylbutyric acid (4-PBA) alleviated HSCs activation and autophagy. In conclusion, these data indicate that depletion of HRC inhibited HSC activation through the ER stress pathway, and HRC may be a potential regulator of liver fibrosis.

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Section: Introductionmentioning

confidence: 99%

Knockdown of histidine-rich calcium binding protein (HRC) suppresses liver fibrosis by inhibiting the activation of hepatic stellate cells

Liu

Gong

et al. 2016

Biology Open

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“…4 ). It has been proved that HRC promotes growth of hepatocellular carcinoma in vitro and in vivo [ 59 ]. Furthermore, HRC also plays a significant role in myocyte differentiation and in anti-apoptotic cardioprotection against ischemia/reperfusion induced cardiac injury [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization and validation of long noncoding RNAs as new candidates in prostate cancer

Zhao

et al. 2020

Cancer Cell Int

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Background Long noncoding RNAs (lncRNAs) have been proved to be an important regulator in gene expression. In almost all kinds of cancers, lncRNAs participated in the process of pathogenesis, invasion, and metastasis. Meanwhile, compared with the large amounts of patients, there is rare knowledge about the role of lncRNAs in prostate cancer (PCa). Material/Method In this study, lncRNA expression profiles of prostate cancer were detected by Agilent microarray chip, 5 pairs of case and control specimens were involved in. Differentially expressed lncRNAs were screened out by volcano plot for constructing lncRNA-miRNA-mRNA central network. Then, the top ten up-regulated and down-regulated lncRNAs were validated by qRT-PCR in another 5 tumor specimens and 7 para-cancerous/benign contrasts. Furthermore, we searched for the survival curve of the top 10 upregulated and downregulated lncRNAs. Results A total of 817 differentially expressed lncRNAs were filtered out by the criteria of fold change (FC) and t-test p < 0.05. Among them, 422 were upregulated, whereas 395 were downregulated in PCa tissues. Gene ontology and KEGG pathway analyses showed that many lncRNAs were implicated in carcinogenesis. lnc-MYL2-4:1 (FC = 0.00141, p = 0.01909) and NR_125857 (FC = 59.27658, p = 0.00128) had the highest magnitude of change. The subsequent qPCR confirmed the expression of NR_125857 was in accordance with the clinical samples. High expression of PCA3, PCAT14 and AP001610.9 led to high hazard ratio while low expression of RP11-279F6.2 led to high hazard ratio. Conclusions Our study detected a relatively novel complicated map of lncRNAs in PCa, which may have the potential to investigate for diagnosis, treatment and follow-up in PCa. Our study revealed the expression of NR_125857 in human PCa tissues was most up-regulated. Further studies are needed to investigate to figure out the mechanisms in PCa.

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“…Our KEGG research demonstrated the Calcium signal pathway referred to PCa (Figure 4). It has been proved that HRC promotes growth of hepatocellular carcinoma in vitro and in vivo (59). Furthermore, HRC also plays a signi cant role in myocyte differentiation and in anti-apoptotic cardioprotection against ischemia/reperfusion induced cardiac injury (60).Intriguingly, the cardiovascular system development, cardiac muscle development, and cardiac muscle hypertrophy were displayed in GO analysis (Figure 4).We speculated the whole eld of muscle, as the part of extracellular matrix component, may make a profound effect on the biological property of PCa.…”

Section: Discussionmentioning

confidence: 99%

Characterization and validation of long noncoding RNAs as new candidates in prostate cancer

Wang

et al. 2020

Preprint

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Background: Long noncoding RNAs (lncRNAs) have been proved to be an important regulator in gene expression. In almost all kinds of cancers, lncRNAs participated in the process of pathogenesis, invasion, and metastasis. Meanwhile, compared with the large amounts of patients, there is rare knowledge about the role of lncRNAs in prostate cancer (PCa). Material/Method: In this study, lncRNA expression profiles of prostate cancer were detected by Agilent microarray chip, 5 pairs of case and control specimens were involved in. Differentially expressed lncRNAs were screened out by volcano plot for constructing lncRNA-miRNA-mRNA central network. Then, the top ten up-regulated and down-regulated lncRNAs were validated by qRT-PCR in another 5 tumor specimens and 7 para-cancerous/benign contrasts. Furthermore, we searched for the survival curve of the top 10 upregulated and downregulated lncRNAs. Results: A total of 817 differentially expressed lncRNAs were filtered out by the criteria of fold change (FC) and t-test p < 0.05. Among them, 422 were upregulated, whereas 395 were downregulated in PCa tissues. Gene ontology and KEGG pathway analyses showed that many lncRNAs were implicated in carcinogenesis. lnc-MYL2-4:1 (FC = 0.00141, p = 0.01909) and NR_125857 (FC = 59.27658, p = 0.00128) had the highest magnitude of change. The subsequent qPCR confirmed the expression of NR_125857 was in accordance with the clinical samples. High expression of PCA3, PCAT14 and AP001610.9 led to high hazard ratio while low expression of RP11-279F6.2 led to high hazard ratio. Conclusions: Our study detected a relatively novel complicated map of lncRNAs in PCa, which may have the potential to investigate for diagnosis, treatment and follow-up in PCa. Our study revealed the expression of NR_125857 in human PCa tissues was most up-regulated. Further studies are needed to investigate to figure out the mechanisms in PCa.

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Histidine‐rich calcium binding protein promotes growth of hepatocellular carcinoma in vitro and in vivo

Cited by 19 publications

References 29 publications

Knockdown of histidine-rich calcium binding protein (HRC) suppresses liver fibrosis by inhibiting the activation of hepatic stellate cells

Knockdown of histidine-rich calcium binding protein (HRC) suppresses liver fibrosis by inhibiting the activation of hepatic stellate cells

Characterization and validation of long noncoding RNAs as new candidates in prostate cancer

Characterization and validation of long noncoding RNAs as new candidates in prostate cancer

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