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Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies

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A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (25 September 2021) | Viewed by 31191

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Dr. Aaron W. Bell

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Department of Pathology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA
Interests: liver cancer; hepatobiliary disease; cirrhosis; fibrosis; liver regeneration

Special Issue Information

Dear Colleagues,

The liver is a vital organ responsible for a myriad of biologic functions, including metabolism, immunity, digestion, detoxification, vitamin storage, production of plasma proteins and clotting factors, and the synthesis of triglycerides, cholesterol, glycogen, and bile acids. A variety of genetic and/or environmental factors, e.g., viruses, diet, alcohol, and microbiome, among others, can result in impaired liver function, steatosis, fatty liver disease, diabetes, cirrhosis, and cancer. Often, these are the result of altered transcriptional regulation of key liver genes and/or gene regulatory networks. Such transcriptional reprogramming has resulted in the discovery of novel biomarkers and therapeutic targets for precision medicine treatments of liver diseases.

The aim of this special issue is to provide an overview of exciting new cutting-edge research in the area of molecular regulation of liver diseases that may garner novel therapeutic targets for precision medicine.

We invite the submission of original research and review articles on molecular regulation of liver diseases, including studies on molecular and cellular mechanisms, molecular functional studies, personalized and precision medicine, biomarker discovery and validation, gene and molecular therapies, and liver disease models.

Dr. Aaron W. Bell
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Non-alcoholic fatty liver disease (NAFLD)
Alcoholic liver disease (ALD)
Hepatocellular carcinoma (HCC)
Cirrhosis
Fibrosis
Viral hepatitis
Type 2 diabetes mellitus

Published Papers (12 papers)

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Editorial

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3 pages, 169 KiB

Open AccessEditorial

Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies

by Aaron W. Bell

J. Pers. Med. 2022, 12(5), 663; https://doi.org/10.3390/jpm12050663 - 21 Apr 2022

Viewed by 1519

Abstract

This Special Issue, entitled “Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies”, includes 11 publications from colleagues working on various liver diseases including non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), hepatocellular carcinoma (HCC), primary biliary cholangitis (PBC), [...] Read more.

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

Research

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19 pages, 6702 KiB

Open AccessArticle

Knockout of Hepatocyte Growth Factor by CRISPR/Cas9 System Induces Apoptosis in Hepatocellular Carcinoma Cells

by Han Ki Lee, Heui Min Lim, See-Hyoung Park and Myeong Jin Nam

J. Pers. Med. 2021, 11(10), 983; https://doi.org/10.3390/jpm11100983 - 29 Sep 2021

Cited by 9 | Viewed by 2303

Abstract

Background: CRISPR/Cas9 system is a prokaryotic adaptive immune response system that uses noncoding RNAs to guide the Cas9 nuclease to induce site-specific DNA cleavage. Hepatocyte growth factor (HGF) is a well-known growth factor that plays a crucial role in cell growth and organ development. According to recent studies, it has been reported that HGF promoted growth of hepatocellular carcinoma (HCC) cells. Here, we investigated the apoptotic effects in HCC cells. Methods: Crispr-HGF plasmid was constructed using GeneArt CRISPR Nuclease Vector. pMex-HGF plasmid that targets HGF overexpressing gene were designed with pMex-neo plasmid. We performed real time-polymerase chain reaction to measure the expression of HGF mRNA. We performed cell counting assay and colony formation assay to evaluate cell proliferation. We also carried out migration assay and invasion assay to reveal the inhibitory effects of Crispr-HGF in HCC cells. Furthermore, we performed cell cycle analysis to detect transfection of Crispr-HGF induced cell cycle arrest. Collectively, we performed annexin V/PI staining assay and Western blot assay. Results: In Crispr-HGF-transfected group, the mRNA expression levels of HGF were markedly downregulated compared to pMex-HGF-transfected group. Moreover, Crispr-HGF inhibited cell viability in HCC cells. We detected that wound area and invaded cells were suppressed in Crispr-HGF-transfected cells. The results showed that transfection of Crispr-HGF induced cell cycle arrest and apoptosis in HCC cells. Expression of the phosphorylation of mitogen activated protein kinases and c-Met protein was regulated in Crispr-HGF-transfected group. Interestingly, we found that the expression of HGF protein in conditioned media significantly decreased in Crispr-HGF-transfected group. Conclusions: Taken together, we found that inhibition of HGF through transfection of Crispr-HGF suppressed cell proliferation and induced apoptotic effects in HCC Huh7 and Hep3B cells. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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10 pages, 877 KiB

Open AccessArticle

Low Preoperative Antithrombin III Level Is Associated with Postoperative Acute Kidney Injury after Liver Transplantation

by Kyoung-Sun Kim, Young-Jin Moon, Sung-Hoon Kim, Bomi Kim, In-Gu Jun, Hye-Mee Kwon, Jun-Gol Song and Gyu-Sam Hwang

J. Pers. Med. 2021, 11(8), 716; https://doi.org/10.3390/jpm11080716 - 26 Jul 2021

Cited by 1 | Viewed by 1836

Abstract

We aimed to determine the association between the preoperative antithrombin III (ATIII) level and postoperative acute kidney injury (AKI) after LT (post-LT AKI). We retrospectively evaluated 2395 LT recipients between 2010 and 2018 whose data of perioperative ATIII levels were available. Patients were divided into two groups based on the preoperative level of ATIII (ATIII < 50% vs. ATIII ≥ 50%). Multivariable regression analysis was performed to assess the risk factors for post-LT AKI. The mean preoperative ATIII levels were 30.2 ± 11.8% in the ATIII < 50% group and 67.2 ± 13.2% in the ATIII ≥ 50% group. The incidence of post-LT AKI was significantly lower in the ATIII ≥ 50% group compared to that in the ATIII < 50% group (54.7% vs. 75.5%, p < 0.001); odds ratio (OR, per 10% increase in ATIII level) 0.86, 95% confidence interval (CI) 0.81–0.92; p < 0.001. After a backward stepwise regression model, female sex, high body mass index, low albumin, deceased donor LT, longer duration of surgery, and high red blood cell transfusion remained significantly associated with post-LT AKI. A low preoperative ATIII level is associated with post-LT AKI, suggesting that preoperative ATIII might be a prognostic factor for predicting post-LT AKI. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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11 pages, 522 KiB

Open AccessArticle

Prognostic Factors in Primary Biliary Cholangitis: A Retrospective Study of Joint Slovak and Croatian Cohort of 249 Patients

by Jakub Gazda, Sylvia Drazilova, Martin Janicko, Ivica Grgurevic, Tajana Filipec Kanizaj, Tomas Koller, Beatrica Bodorovska, Tonci Bozin, Maja Mijic, Zrinka Rob, Ivana Mikolasevic, Anita Madir, Branislav Kucinsky and Peter Jarcuska

J. Pers. Med. 2021, 11(6), 495; https://doi.org/10.3390/jpm11060495 - 01 Jun 2021

Cited by 3 | Viewed by 2271

Abstract

Objective: To identify pretreatment laboratory parameters associated with treatment response and to describe the relationship between treatment response and liver decompensation in patients with primary biliary cholangitis treated with ursodeoxycholic acid. Methods: We defined treatment response as both ALP ≤ 1.67 × ULN and total bilirubin ≤ 2 × ULN. Multiple logistic regression analyses were performed to adjust for confounding effects of sociodemographic variables. Results: Pretreatment total bilirubin ((TB); OR = 0.3388, 95%CI = 0.1671–0.6077), ALT (OR = 0.5306, 95%CI = 0.3830–0.7080), AST (OR = 0.4065, 95%CI = 0.2690–0.5834), ALP (OR = 0.3440, 95%CI = 0.2356–0.4723), total cholesterol ((TC); OR = 0.7730, 95%CI = 0.6242–0.9271), APRI (OR = 0.3375, 95%CI = 0.1833–0.5774), as well as pretreatment albumin (OR = 1.1612, 95%CI = 1.0706–1.2688) and ALT/ALP (OR = 2.4596, 95%CI = 1.2095–5.5472) were associated with treatment response after six months of treatment. Pretreatment TB (OR = 0.2777, 95%CI = 0.1288–0.5228), ALT (OR = 0.5968, 95%CI = 0.4354–0.7963), AST (OR = 0.4161, 95%CI = 0.2736–0.6076), ALP (OR = 0.4676, 95%CI = 0.3487–0.6048), APRI (OR = 0.2838, 95%CI = 0.1433–0.5141), as well as pretreatment albumin (OR = 1.2359, 95%CI = 1.1257–1.3714) and platelet count (OR = 1.0056, 95%CI = 1.0011–1.0103) were associated with treatment response after 12 months of treatment. Treatment response after 6 months of UDCA therapy is significantly associated with treatment response after 12 months of UDCA therapy (OR = 25.2976, 95% CI = 10.5881–68.4917). Treatment responses after 6 and 12 months of UDCA therapy decrease the risk of an episode of liver decompensation in PBC patients (OR = 12.1156, 95%CI = 3.7192–54.4826 and OR = 21.6000, 95%CI = 6.6319–97.3840, respectively). Conclusions: There are several pretreatment laboratory parameters associated with treatment response in patients with primary biliary cholangitis. Treatment response after six months is significantly associated with treatment response after 12 months of ursodeoxycholic acid (UDCA) therapy. Treatment responses after 6 and 12 months of UDCA decrease the risk of an episode of liver decompensation. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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14 pages, 3748 KiB

Open AccessArticle

A Bioinformatics Analysis Identifies the Telomerase Inhibitor MST-312 for Treating High-STMN1-Expressing Hepatocellular Carcinoma

by Szu-Jen Wang and Pei-Ming Yang

J. Pers. Med. 2021, 11(5), 332; https://doi.org/10.3390/jpm11050332 - 22 Apr 2021

Cited by 7 | Viewed by 2666

Abstract

Hepatocellular carcinoma (HCC) is a relatively chemo-resistant tumor. Several multi-kinase inhibitors have been approved for treating advanced HCC. However, most HCC patients are highly refractory to these drugs. Therefore, the development of more effective therapies for advanced HCC patients is urgently needed. Stathmin 1 (STMN1) is an oncoprotein that destabilizes microtubules and promotes cancer cell migration and invasion. In this study, cancer genomics data mining identified STMN1 as a prognosis biomarker and a therapeutic target for HCC. Co-expressed gene analysis indicated that STMN1 expression was positively associated with cell-cycle-related gene expression. Chemical sensitivity profiling of HCC cell lines suggested that High-STMN1-expressing HCC cells were the most sensitive to MST-312 (a telomerase inhibitor). Drug–gene connectivity mapping supported that MST-312 reversed the STMN1-co-expressed gene signature (especially BUB1B, MCM2/5/6, and TTK genes). In vitro experiments validated that MST-312 inhibited HCC cell viability and related protein expression (STMN1, BUB1B, and MCM5). In addition, overexpression of STMN1 enhanced the anticancer activity of MST-312 in HCC cells. Therefore, MST-312 can be used for treating STMN1-high expression HCC. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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13 pages, 8166 KiB

Open AccessArticle

Preclinical Application of Reduced Manipulated Processing Strategy to Collect Transplantable Hepatocytes: A Pilot and Feasibility Study

by Ya-Hui Chen, Hui-Ling Chen, Cheng-Maw Ho, Hung-Yen Chen, Shu-Li Ho, Rey-Heng Hu, Po-Huang Lee and Mei-Hwei Chang

J. Pers. Med. 2021, 11(5), 326; https://doi.org/10.3390/jpm11050326 - 21 Apr 2021

Cited by 1 | Viewed by 1622

Abstract

Background: The complex isolation and purification process of hepatocytes for transplantation is labor intensive and with great contamination risk. Here, as a pilot and feasibility study, we examined in vitro and in vivo hepatocyte isolation feasibility and cell function of Cell Saver^® Elite^®, an intraoperative blood-cell-recovery system. Methods: Rat and pig liver cells were collected using this system and then cultured in vitro, and their hepatocyte-specific enzymes were characterized. We then transplanted the hepatocytes in an established acute liver–injured (retrorsine+D-galactosamine-treated) rat model for engraftment. Recipient rats were sacrificed 1, 2, and 4 weeks after transplantation, followed by donor-cell identification and histological, serologic, and immunohistopathological examination. To demonstrate this Cell Saver^® strategy is workable in the first place, traditional (classical) strategy, in our study, behaved as certainty during the cell manufacturing process for monitoring quality assurance throughout the course, from the start of cell isolation to post-transplantation. Results: We noted that in situ collagenase perfusion was followed by filtration, centrifugation, and collection in the Cell Saver^® until the process ended. Most (>85%) isolated cells were hepatocytes (>80% viability) freshly demonstrating hepatocyte nuclear factor 4α and carbamoyl-phosphate synthase 1 (a key enzyme in the urea cycle), and proliferating through intercellular contact in culture, with expression of albumin and CYP3A4. After hepatocyte transplantation in dipeptidyl peptidase IV (−/−) rat liver, wild-type donor hepatocytes engrafted and repopulated progressively in 4 weeks with liver functional improvement. Proliferating donor hepatocyte–native biliary ductular cell interaction was identified. Post-transplantation global liver functional recovery after Cell Saver and traditional methods was comparable. Conclusions: Cell Saver^® requires reduced manual manipulation for isolating transplantable hepatocytes. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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14 pages, 2358 KiB

Open AccessArticle

Animal Evidence for Synergistic Induction of Hepatic Injury by Dietary Fat and Alcohol Consumption and Its Potential Mechanisms

by Hyeong-Geug Kim, Jing-Hua Wang, Hyo-Seon Kim, Jin-Seok Lee, Hwi-Jin Im, Sung-Bae Lee, Dong-soo Lee, Gang-Min Hur and Chang-Gue Son

J. Pers. Med. 2021, 11(4), 287; https://doi.org/10.3390/jpm11040287 - 08 Apr 2021

Cited by 2 | Viewed by 1976

Abstract

In contrast to nonalcoholic fatty liver disease (NAFLD), metabolic-associated fatty liver disease (MAFLD) as an innovative definition can coexist with significant alcohol consumption. Massive clinical observations have indicated that high-fat/-calorie diet induced metabolic dysfunction along with alcohol intake deteriorates steatotic liver injury. To explore the potential mechanisms of fatty diet together with alcohol-induced steatohepatitis, we adopted a rat model by comparing a half-dose combination of fat diet (20%) and alcohol (10%) with their corresponding double dose of 40% fat diet and 20% alcohol for 8 weeks. The notable alterations in histopathology, acceleration in the oxidation parameters (ROS, NO and lipid peroxidation) and serum transaminase levels were shown in the concomitant group. Concomitant use of a high-fat diet and alcohol provoked hepatic endoplasmic reticulum stress, but did not activate mitochondria-mediated apoptosis parameters compared to F. In contrast, the notable activation of caspase-12 and nuclear translocation of CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) were observed only in the combined treatment group. The concomitant dietary fat intake and alcohol consumption lead to liver injury initially and later to steatohepatitis by the overdose of fat or alcohol, and in which the CHOP and caspase-12 might be involved in synergistic acceleration of steatohepatitis through a mitochondria-independent manner. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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11 pages, 1172 KiB

Open AccessArticle

Long-Term Tacrolimus Blood Trough Level and Patient Survival in Adult Liver Transplantation

by Chih-Yang Hsiao, Ming-Chih Ho, Cheng-Maw Ho, Yao-Ming Wu, Po-Huang Lee and Rey-Heng Hu

J. Pers. Med. 2021, 11(2), 90; https://doi.org/10.3390/jpm11020090 - 01 Feb 2021

Cited by 6 | Viewed by 2795

Abstract

Tacrolimus is the most widely used immunosuppressant in liver transplant (LT) patients. However, the ideal long-term target level for these patients is unknown. This retrospective study aimed to investigate the impact of tacrolimus blood concentration five years after LT on long-term patient survival outcomes in adult LT recipients. Patients who underwent LT between January 2004 and July 2014 at a tertiary medical center were included in this study (n = 189). The mean tacrolimus blood concentrations of each patient during the fifth year after LT were recorded and the overall survival rate was determined. A multivariate analysis of factors associated with long-term survival was conducted using a Cox’s model. The median follow-up period was 9.63 years, and 144 patients (76.2%) underwent live donor LT. Sixteen patients died within 5 years of LT. In the Cox’s model, patients with a mean tacrolimus blood trough level of 4.6–10.2 ng/mL had significantly better long-term survival than those with a mean tacrolimus blood trough level outside this range (estimated hazard ratio = 4.76; 95% confidence interval: 1.34–16.9, p = 0.016). Therefore, a tacrolimus level no lower than 4.6 ng/mL would be recommended in adult LT patients. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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15 pages, 1474 KiB

Open AccessArticle

Dynamic Prognostication in Transplant Candidates with Acute-on-Chronic Liver Failure

by Cheng-Yueh Lu, Chi-Ling Chen, Cheng-Maw Ho, Chih-Yang Hsiao, Yao-Ming Wu, Ming-Chih Ho, Po-Huang Lee and Rey-Heng Hu

J. Pers. Med. 2020, 10(4), 230; https://doi.org/10.3390/jpm10040230 - 15 Nov 2020

Cited by 6 | Viewed by 1630

Abstract

We aimed to extensively investigate clinical markers that are sufficiently dynamic for prognosis of acute-on-chronic liver failure (ACLF). Defined by the Asian Pacific Association for the Study of the Liver (APASL) criteria, patients with ACLF on the liver transplant waitlist in a tertiary center were retrospectively reviewed. Laboratory results and severity scores at three time points (days 1, 7, and 14 after admission) were analyzed. From 2015 to 2019, 64 patients with ACLF were enrolled, of which 24 received a liver transplant from 22 live donors. The hospital mortality rate was 31% (8% for transplant; 45% for nontransplant groups), and the 3-month survival was crucial for determining long-term outcomes. The number of significant variables for mortality, and, specifically, the hazards of international normalized ratio of prothrombin time (INR) and APASL ACLF Research Consortium (AARC) score were increased within two weeks. In multivariable analysis, INR and AARC score (D-14) were associated with poor survival and liver transplant was a protective factor in all patients, while AARC score (D-14) was significant in the nontransplant group. AARC score at day 14 is an independent risk factor for mortality in ACLF. Liver transplant from live donors reversed poor outcomes in patients with ACLF in a timely manner. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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Review

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12 pages, 807 KiB

Open AccessFeature PaperReview

Is HSD17B13 Genetic Variant a Protector for Liver Dysfunction? Future Perspective as a Potential Therapeutic Target

by Takashi Motomura, Sriram Amirneni, Ricardo Diaz-Aragon, Lanuza A. P. Faccioli, Michelle R. Malizio, Michael C. Coard, Zehra N. Kocas-Kilicarslan, Carla Frau, Nils Haep, Alina Ostrowska, Rodrigo M. Florentino and Alejandro Soto-Gutierrez

J. Pers. Med. 2021, 11(7), 619; https://doi.org/10.3390/jpm11070619 - 30 Jun 2021

Cited by 10 | Viewed by 4506

Abstract

As diet and lifestyle have changed, fatty liver disease (FLD) has become more and more prevalent. Many genetic risk factors, such as variants of PNPLA3, TM6SF2, GCKR, and MBOAT7, have previously been uncovered via genome wide association studies (GWAS) to be associated with FLD. In 2018, a genetic variant (rs72613567, T > TA) of hydroxysteroid 17-β dehydrogenase family 13 (HSD17B13) was first associated with a lower risk of developing alcoholic liver disease and non-alcoholic fatty liver disease (NAFLD) in minor allele carriers. Other HSD17B13 variants were also later linked with either lower inflammation scores among NAFLD patients or protection against NAFLD (rs6834314, A > G and rs9992651, G > A) respectively. HSD17B13 is a lipid droplet-associated protein, but its function is still ambiguous. Compared to the other genetic variants that increase risk for FLD, HSD17B13 variants serve a protective role, making this gene a potential therapeutic target. However, the mechanism by which these variants reduce the risk of developing FLD is still unclear. Because studies in cell lines and mouse models have produced conflicting results, human liver tissue modeling using induced pluripotent stem cells may be the best way to move forward and solve this mystery. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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19 pages, 1209 KiB

Open AccessFeature PaperReview

Target Therapies for NASH/NAFLD: From the Molecular Aspect to the Pharmacological and Surgical Alternatives

by Michele Finotti, Maurizio Romano, Pasquale Auricchio, Michele Scopelliti, Marco Brizzolari, Ugo Grossi, Marco Piccino, Stefano Benvenuti, Giovanni Morana, Umberto Cillo and Giacomo Zanus

J. Pers. Med. 2021, 11(6), 499; https://doi.org/10.3390/jpm11060499 - 02 Jun 2021

Cited by 8 | Viewed by 3554

Abstract

Non-alcoholic fatty liver disease represents an increasing cause of chronic hepatic disease in recent years. This condition usually arises in patients with multiple comorbidities, the so-called metabolic syndrome. The therapeutic options are multiple, ranging from lifestyle modifications, pharmacological options, to liver transplantation in selected cases. The choice of the most beneficial one and their interactions can be challenging. It is mandatory to stratify the patients according to the severity of their disease to tailor the available treatments. In our contribution, we review the most recent pharmacological target therapies, the role of bariatric surgery, and the impact of liver transplantation on the NAFLD outcome. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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19 pages, 2612 KiB

Open AccessReview

New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics

by Ya-Ling Yang, Yen-Hsiang Chang, Chia-Jung Li, Ying-Hsien Huang, Ming-Chao Tsai, Pei-Yi Chu and Hung-Yu Lin

J. Pers. Med. 2021, 11(3), 219; https://doi.org/10.3390/jpm11030219 - 18 Mar 2021

Cited by 15 | Viewed by 2813

Abstract

Hepatocellular carcinoma (HCC) remains one of the most lethal human cancer globally. For advanced HCC, curable plan for advanced HCC is yet to be established, and the prognosis remains poor. The detail mechanisms underlying the progression of HCC tumorigenicity and the corruption of tumor microenvironment (TME) is complex and inconclusive. A growing body of studies demonstrate microRNAs (miRs) are important regulators in the tumorigenicity and TME development. Notably, mounting evidences indicate miR-29a play a crucial role in exerting hepatoprotective effect on various types of stress and involved in the progression of HCC, which elucidates their potential theragnostic implications. In this review, we reviewed the advanced insights into the detail mechanisms by which miR-29a dictates carcinogenesis, epigenetic program, and metabolic adaptation, and implicated in the sponging activity of competitive endogenous RNAs (ceRNA) and the TME components in the scenario of HCC. Furthermore, we highlighted its clinical significance in diagnosis and prognosis, as well as the emerging therapeutics centered on the activation of miR-29a. Full article

(This article belongs to the Special Issue Personalized Medicine for Liver Disease: From Molecular Mechanisms to Potential Targeted Therapies)

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