Decreased expression of autophagy-related proteins in malignant epithelial ovarian cancer

Shen, Yang; Li, Dan Dan; Wang, Lin Lin; Deng, Rong; Zhu, Xiao Feng

doi:10.4161/auto.6827

Cited by 183 publications

(146 citation statements)

References 15 publications

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“…While a similar decrease in MAP1LC3A expression was reported in cerebral and ovarian cancer, 39,40 in other malignancies, such as esophageal and gastrointestinal carcinomas, an increased LC3 expression was prevailing. 41 There were also reports connecting an increased LC3 activity with poor outcome in pancreatic tumors and with a better survival in glioblastoma patients with poor performance score.…”

Section: Discussionsupporting

confidence: 68%

“…Such decreased cytoplasmic expression of BECN1 has been correlated with tumor progression in breast, ovarian, and cerebral neoplasms 39,46,47 and with a reduced survival rate in neoplasms of esophageal, colorectal, hepatocellular, and cerebral origin. [48][49][50][51] Liang et al 46 explained this immunohistochemical decline in cytoplasmic expression of the protein in terms of BECN1 inactivation and loss of its tumor suppressor functions.…”

Section: Discussionmentioning

confidence: 97%

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Autophagy patterns and prognosis in uveal melanomas

et al. 2011

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Autophagy is a self-degradation mechanism by which cells recycle their own cytoplasmic constituents. It has been claimed that, under certain conditions, such a process may be associated with tumor progression. In this study, the autophagic activity was investigated in a series of 99 uveal melanomas after immunohistochemical staining for the autophagy-associated proteins MAP1LC3A and BECN1, most commonly known as LC3A and Beclin 1, respectively. These were assessed in parallel with the hypoxia-inducible factor 1a (HIF1A) and its downstream protein lactate dehydrogenase 5 (composed by five LDHA subunits). Increased autophagic reactivity, detected by MAP1LC3A or BECN1, was associated with intense pigmentation and tumor hypoxia. Uveal melanomas with extensive overexpression of BECN1 or those with underexpression of this protein were associated with the worst prognosis, but the former manifested metastases much earlier than the latter; only 58% of patients with extensive BECN1 overexpression were alive at 4 years, compared with 80% of patients with underexpressed patterns. It is concluded that autophagy is commonly upregulated in uveal melanomas, and may be associated with hypoxia and intense pigmentation. There is a strong association between extensive BECN1 overexpression and early metastases/poor prognosis, and between underexpression of this protein and late metastases/better prognosis.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 97%

Autophagy patterns and prognosis in uveal melanomas

et al. 2011

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“…39 Decreased expression of beclin 1 has also been demonstrated in some human cancers, including glioblastomas, ovarian cancers and esophageal cancers. [39][40][41] However, increased expression of beclin 1 has been reported in colorectal and gastric cancer cells as compared with the normal counterparts. 42 In this study, we found that beclin 1 mRNA was marked highly expression in 85% clinical ICC samples and 76% cases showed high protein expression.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of active autophagy induces apoptosis and increases chemosensitivity in cholangiocarcinoma

Hou

Dong

Tan

et al. 2011

Laboratory Investigation

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Intrahepatic cholangiocellular carcinomas (ICCs) are usually fatal neoplasms originating from bile duct epithelia. However, many cholangiocarcinoma cells are shown to be resistant to chemotherapeutic drugs, which induce cell apoptosis. The role of autophagy and the therapeutic value of autophagy-associated genes are largely unknown in ICC. Here, we showed that autophagy was activated in nutrient starvation and xenograft cholangiocarcinoma cells. Furthermore, expression of autophagic genes and their autophagic activity were higher in clinical ICC specimens than that in normal cholangiocytes separated by laser capture microdissection. Inhibition of autophagy by autophagy inhibitors or siRNA, cholangiocarcinoma cells showed detention of proliferation and increase of apoptosis during nutrient starvation. In addition, autophagy inhibitor treatment or knockdown of beclin 1 suppressed tumor growth and sensitized ICC cells to chemotherapeutic agent-induced cell death. In conclusion, our data showed that autophagy is activated in ICC, and inactivation of autophagy may lead to cell apoptosis and enhance chemotherapy sensitivity. Intrahepatic cholangiocellular carcinoma (ICC) is a malignant neoplasm originating from epithelium of the biliary tree with high mortality. 1 ICC accounts for 5-30% of all primary liver malignancies, and its incidence has been increasing over the last several decades. 2 The mortality from intrahepatic cholangiocarcinoma is very high, with the 5-year survival rates being o15-20% in most series. 3,4 However, the exact molecular mechanisms of biliary epithelium malignant transformation are not well understood. Despite improved diagnostic and operative techniques, the prognosis of ICC remains poor. 5 Indeed, ICC is a type of cancer highly resistant to conventional antineoplastic medicines, 4 which is partially attributed to the property of insensitivity to cell death induced by cytotoxic agents. It is well known that the avoidance of apoptosis is one of the hallmarks of cancer cells, 6 and that failure to induce apoptosis by anticancer treatments contributes to chemotherapeutic failure and tumor progression. Although autophagy, an alternative caspase-independent cell death program, 7 is thought to be used for cancer treatment, its underlying molecular mechanism is still controversial in antineoplastic therapy and also in tumor progression.Autophagy is a conserved catabolic process by which cells themselves digest their organelles. 8 Autophagy has emerged as a homeostatic mechanism regulating the turnover of long-lived or damaged proteins and organelles, and buffering metabolic stress induced under starvation conditions by recycling intracellular constituents. 9 Autophagosomes engulfing organelles then fuse with lysosomes and mature into autolysosomes. Autophagic processes have been well characterized in yeast, and 430 autophagy-related genes that encode the proteins executing autophagy have been identified in the field of yeast genetics. 6,7 The amino acids and fatty acids generated by autophagic degr...

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“…It was one of the first autophagy proteins to be related to malignancies (31). Beclin-1 functions as a tumor suppressor in breast and ovarian cancers and glioblastomas and is associated with tumorigenesis in colorectal and gastric cancers (32)(33)(34). Because beclin-1 can influence apoptosis and cellular hyperproliferation, it may have a role in NP.…”

Section: Discussionmentioning

confidence: 99%

Expression profiles of CD11b, galectin-1, beclin-1, and caspase-3 in nasal polyposis*

Dilci¹,

Varol²,

Kılıçcıoğlu³

et al. 2017

Turk J Med Sci

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Background/aim: Nasal polyposis is a chronic inflammatory disease affecting the paranasal sinuses and nasal mucosae. It is thought that genetic and molecular mechanisms in inflammatory and apoptotic pathways are the main factors in the etiopathogenesis of nasal polyposis. The aim of this study was to investigate the expression patterns of CD11b, galectin-1, beclin-1, and caspase-3 in nasal polyps. Materials and methods:The mRNA expression levels of CD11b, galectin-1, beclin-1, and caspase-3 protein and western blot analysis of caspase-3 protein were evaluated in inferior turbinate mucosae and nasal polyp tissues.Results: CD11b expression was markedly higher in nasal polyp tissues when compared to turbinate mucosae (5.5 times higher, P < 0.05). Expression of galectin-1 was not statistically higher in nasal polyp tissues when compared to the controls. Beclin-1 expression in nasal polyp tissues was lower than in controls (17 times lower, P < 0.05). Caspase-3 expression was significantly lower in nasal polyp tissues than in controls (5.5 times lower, P < 0.05). Conclusion:Inflammation, apoptosis, and hyperproliferation are the major cellular processes in nasal polyposis and these proteins may take part and play some important roles in formation of this disease and the targeting of new treatment protocols.

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Decreased expression of autophagy-related proteins in malignant epithelial ovarian cancer

Cited by 183 publications

References 15 publications

Autophagy patterns and prognosis in uveal melanomas

Autophagy patterns and prognosis in uveal melanomas

Inhibition of active autophagy induces apoptosis and increases chemosensitivity in cholangiocarcinoma

Expression profiles of CD11b, galectin-1, beclin-1, and caspase-3 in nasal polyposis*

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