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We began analyzing https://www.oncotarget.com/article/16685/text/, but it redirected us to https://www.oncotarget.com/article/16685/text/. The analysis below is for the second page.

Title[redir]:
Chaperone-mediated autophagy compensates for impaired macroautophagy in the cirrhotic liver to promote hepatocellular carcinoma | Oncotarget
Description:
// Srinivas Chava 1 , Christine Lee 1 , Yucel Aydin 2 , Partha K. Chandra 1 , Asha Dash 1 , Milad Chedid 1 , Swan N. Thung 3 , Krzysztof Moroz 1 , Tong Wu 1 , Nabeen C. Nayak 4 and Srikanta Dash 1 1 Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, Louisiana, USA 2 Department of Medicine, Division of Gastroenterology and Hepatology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA 3 The Lillian and Henry M. Stratton-Hans Popper Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, USA 4 Senior Consultant and Advisor, Sir Ganga Ram Hospital, Department of Pathology, New Delhi, India Correspondence to: Srikanta Dash, email: // Keywords : liver cirrhosis, hepatocellular carcinoma, macroautophagy, chaperone-mediated autophagy, endoplasmic reticulum, Pathology Section Received : January 12, 2017 Accepted : March 19, 2017 Published : March 29, 2017 Abstract Macroautophagy and chaperone-mediated autophagy (CMA) represent two major lysosomal degradation processes and often compensate for one another to facilitate cell survival. The aim of this study was to determine whether these autophagy pathways could compensate for one another to promote HCC cell survival in the cirrhotic liver. Analysis of normal liver tissue showed no expression of glypican-3 or p62 proteins, suggesting that macroautophagy is the major contributor to autophagic flux under non-pathological conditions. Of 46 cirrhotic livers with HCC examined, 39 (84%) of HCCs showed increased expression of p62, and 36 (78%) showed increased expression of glypican-3, while adjacent non-tumorous hepatocytes were negative for expression of p62 and glypican-3, similar to normal liver tissue. These results suggest that macroautophagy flux is impaired in HCC. Furthermore, more than 95% of HCCs showed altered expression of LAMP-2A compared to the surrounding non-tumorous cirrhotic liver, consistent with induction of CMA in HCC. Elevated expression of glucose-regulated protein 78 (GRP78) and heat shock cognate protein (Hsc70) were detected in 100% of HCC and adjacent non-tumorous cirrhotic livers, suggesting that unresolved ER-stress is associated with HCC risk in liver cirrhosis. Interestingly, inhibition of lysosomal degradation using hydroxychloroquine (HCQ) induced expression of the tumor suppressor p53, promoted apoptosis, and inhibited HCC growth, whereas activation of autophagy using an mTOR inhibitor (Torin1) promoted HCC growth. Results of this study suggest that induction of CMA compensates for the impairment of macroautophagy to promote HCC survival in the cirrhotic liver.

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Keywords {🔍}

hcc, liver, expression, cirrhotic, lampa, staining, cells, autophagy, macroautophagy, cma, cirrhosis, figure, cell, hccs, nontumorous, hepatocellular, glypican, impaired, protein, survival, livers, carcinoma, cancer, torin, showed, adjacent, stress, tissue, hcq, positive, induced, tumor, disease, increased, compared, intensity, high, found, hours, viral, samples, etiologies, lysosomal, grp, hsc, study, treatment, score, proliferation, negative,

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conventional fda-approved chemotherapy national age-sex specific wnt/β-catenin pathway [30] inaugural editorial mtorc2-akt pathway [35] single-span membrane protein stratton-hans popper department kaplan-meier survival analysis paraffin-embedded tissue sections called mallory-denk bodies open-access journal dedicated bravo-san pedro jm protein-hsc70 complex binds vesicle-mediated autophagy switches lysosomal receptor lamp-2a lamp-2a staining patterns cma-related protein expressions high-grade dysplastic nodules stress protein aggregates/deposits alter lamp-2a expression stresses hcc-initiating cells cma-mediated protein degradation ethanol-exposed liver disease liver ischemia-perfusion injury publication alerts subscribe low-basal level activation pro-survival pathways maintained chaperone-mediated autophagy compensates lamp-2a expression varied inhibit lamp-2a expression lamp-2a staining pattern lamp-2a expression increased increased lamp-2a expression mallory-denk bodies present nonessential amino acids current models suggest obesity-related hepatocellular carcinoma detected lamp-2a expression low lamp-2a expression annu rev nutr unresolved er-stress free publication glucose-regulated protein 78 er-stress/upr activation heat shock proteins interferon-alpha-induced hepatitis develop hepatic neoplasia perk-mediated degradation flow cytometry analysis serum free medium

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Does chemotherapy prevent HCV-related hepatocellular carcinoma?
Molecularly targeted therapy for advanced hepatocellular carcinoma - a drug development crisis?

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Article:
      license:https://creativecommons.org/licenses/by/4.0/
      publisher:
         type:Organization
         name:Oncotarget
         logo:
            type:ImageObject
            url:https://www.oncotarget.com/images/oncotarget-logo-square.png
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      dateModified:2017-06-19T11:23:52Z
      mainEntityOfPage:
         type:WebPage
         id:https://www.oncotarget.com/article/16685/text/
      headline:Chaperone-mediated autophagy compensates for impaired macroautophagy in the cirrhotic liver to promote hepa
      articleSection:Research Papers: Pathology
      sameAs:https://doi.org/10.18632/oncotarget.16685
      image:https://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=viewFile&path%5B%5D=16685&path%5B%5D=53363&path%5B%5D=244984
      datePublished:2017-03-29T00:00:00Z
      author:
            type:Person
            name:Chava, Srinivas
            type:Person
            name:Lee, Christine
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            name:Aydin, Yucel
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            name:Dash, Asha
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            name:Chedid, Milad
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            name:Thung, Swan N.
            type:Person
            name:Moroz, Krzysztof
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            name:Wu, Tong
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            name:Nayak, Nabeen C.
            type:Person
            name:Dash, Srikanta
Organization:
      name:Oncotarget
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         url:https://www.oncotarget.com/images/oncotarget-logo-square.png
         width:1200
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ImageObject:
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      width:1200
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WebPage:
      id:https://www.oncotarget.com/article/16685/text/
Person:
      name:Chava, Srinivas
      name:Lee, Christine
      name:Aydin, Yucel
      name:Chandra, Partha K.
      name:Dash, Asha
      name:Chedid, Milad
      name:Thung, Swan N.
      name:Moroz, Krzysztof
      name:Wu, Tong
      name:Nayak, Nabeen C.
      name:Dash, Srikanta

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