RETRACTED ARTICLE: Tumour-originated exosomal miR-155 triggers cancer-associated cachexia to promote tumour progression

Wu, Qi; Sun, Si; Li, Zhiyu; Yang, Qian; Li, Bei; Zhu, Shan; Wang, Lijun; Yuan, Jingping; Yang, Chuanfang; Li, Juanjuan

doi:10.1186/s12943-018-0899-5

Cited by 101 publications

(119 citation statements)

References 9 publications

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“…Numerous studies have revealed that miRNA is intimately related to tumor initiation and progression. 38,39 Present works have confirmed that miR-31 is downregulated in liver cancer and involved in liver cancer cell apoptosis, migration impairment, and proliferation delay. 10,40 But the underlying mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 84%

<p>miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways</p>

Zhang¹,

Xu²,

Yang³

2020

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Purpose: Liver cancer is one of the most common malignant tumor in the world. miR-31 is downregulated in liver cancer and associated with tumor growth and metastasis. However, the underlying mechanism remains unclear. Methods: Cellular apoptosis was detected via MTT, TUNEL assay, LDH release and Annexin V/PI flow-cytometry analysis. Cellular migration and invasion were measured by the Transwell chamber assay. Mitochondrial functions were evaluated via mitochondrial membrane potential JC-1 staining and mPTP opening assessment. The mitophagy activity was examined via Western blots. Results: In the present study, our results confirm that miR-31 promotes apoptosis and inhibits proliferation and metastasis in liver cancer HepG2 cells. In vitro, miR-31 promotes HepG2 cell apoptosis through the mitochondrial pathway as indicated by mitochondrial potential reduction, increased mPTP opening time, cty-c release and imbalance of pro-and anti-apoptotic proteins. Furthermore, miR-31 reduces the energy generation by inhibiting mitochondrial respiratory function. At last, it is demonstrated that miR-31 triggers the mitochondrial damage via ROCK1/F-actin pathway. Inhibiting the ROCK1/F-actin pathway abolishes the effects of miR-31 mimic on mitochondrial injury, apoptosis, proliferation arrest and migration inhibition. Conclusion: Our results reveal that miR-31 can inhibit HepG2 cell survival and metastasis by activating the ROCK1/F-actin pathway.

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Section: Discussionmentioning

confidence: 84%

<p>miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways</p>

Zhang¹,

Xu²,

Yang³

2020

OTT

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“…In addition to CAFs and MSCs, other noncancerous cells are influenced by tumor-derived EV-RNAs to disrupt their normal phenotypes. EV-miR-155 from BC cells could promote brown differentiation and catabolism of adipocytes by targeting PPARγ [168]. Tumorderived EV-miR-21 promotes apoptosis of skeletal muscle cells by activating TLR7 [169].…”

Section: Regulation Of Malignant Phenotypes Of Cancer Cells By Tumor mentioning

confidence: 99%

Comprehensive landscape of extracellular vesicle-derived RNAs in cancer initiation, progression, metastasis and cancer immunology

et al. 2020

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Extracellular vesicles (EVs), a class of heterogeneous membrane vesicles, are generally divided into exosomes and microvesicles on basis of their origination from the endosomal membrane or the plasma membrane, respectively. EV-mediated bidirectional communication among various cell types supports cancer cell growth and metastasis. EVs derived from different cell types and status have been shown to have distinct RNA profiles, comprising messenger RNAs and non-coding RNAs (ncRNAs). Recently, ncRNAs have attracted great interests in the field of EV-RNA research, and growing numbers of ncRNAs ranging from microRNAs to long ncRNAs have been investigated to reveal their specific functions and underlying mechanisms in the tumor microenvironment and premetastatic niches. Emerging evidence has indicated that EV-RNAs are essential functional cargoes in modulating hallmarks of cancers and in reciprocal crosstalk within tumor cells and between tumor and stromal cells over short and long distance, thereby regulating the initiation, development and progression of cancers. In this review, we discuss current findings regarding EV biogenesis, release and interaction with target cells as well as EV-RNA sorting, and highlight biological roles and molecular mechanisms of EV-ncRNAs in cancer biology.

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“…Yet, mir-155-5p secreted by human breast cancer cells was proven to promote WAT browning and increased BAT thermogenesis but not lean mass loss. This was due to the targeting of peroxisome proliferatoractivated receptor gamma (PPARγ), a well-known regulator of glucose metabolism and fatty acid storage (69).…”

Section: Micrornasmentioning

confidence: 99%

Management of Cancer Cachexia: Attempting to Develop New Pharmacological Agents for New Effective Therapeutic Options

2020

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Cancer cachexia (CC) is a multifactorial syndrome characterized by systemic inflammation, uncontrolled weight loss and dramatic metabolic alterations. This includes myofibrillar protein breakdown, increased lipolysis, insulin resistance, elevated energy expediture, and reduced food intake, hence impairing the patient's response to anti-cancer therapies and quality of life. While a decade ago the syndrome was considered incurable, over the most recent years much efforts have been put into the study of such disease, leading to the development of potential therapeutic strategies. Several important improvements have been reached in the management of CC from both the diagnostic-prognostic and the pharmacological viewpoint. However, given the heterogeneity of the disease, it is impossible to rely only on single variables to properly treat patients presenting this metabolic syndrome. Moreover, the cachexia symptoms are strictly dependent on the type of tumor, stage and the specific patient's response to cancer therapy. Thus, the attempt to translate experimentally effective therapies into the clinical practice results in a great challenge. For this reason, it is of crucial importance to further improve our understanding on the interplay of molecular mechanisms implicated in the onset and progression of CC, giving the opportunity to develop new effective, safe pharmacological treatments. In this review we outline the recent knowledge regarding cachexia mediators and pathways involved in skeletal muscle (SM) and adipose tissue (AT) loss, mainly from the experimental cachexia standpoint, then retracing the unimodal treatment options that have been developed to the present day.

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RETRACTED ARTICLE: Tumour-originated exosomal miR-155 triggers cancer-associated cachexia to promote tumour progression

Cited by 101 publications

References 9 publications

<p>miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways</p>

<p>miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways</p>

Comprehensive landscape of extracellular vesicle-derived RNAs in cancer initiation, progression, metastasis and cancer immunology

Management of Cancer Cachexia: Attempting to Develop New Pharmacological Agents for New Effective Therapeutic Options

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