Subpixel motion artifacts correction and motion estimation for 3D-OCT.

A number of hardware-based and software-based strategies have been suggested to eliminate motion artifacts for improvement of 3D-optical coherence tomography (OCT) image quality. However, the hardware-based strategies have to employ additional hardware to record motion compensation information. Many software-based strategies have to need additional scanning for motion correction at the expense of longer acquisition time. To address this issue, we propose a motion artifacts correction and motion estimation method for OCT volumetric imaging of anterior segment, without requirements of additional hardware and redundant scanning. The motion correction effect with subpixel accuracy for in vivo 3D-OCT has been demonstrated in experiments. Moreover, the physiological information of imaging object, including respiratory curve and respiratory rate, has been experimentally extracted using the proposed method. The proposed method offers a powerful tool for scientific research and clinical diagnosis in ophthalmology and may be further extended for other biomedical volumetric imaging applications.

Dorsomorphin attenuates ABCG2-mediated multidrug resistance in colorectal cancer.

Colorectal cancer is a common malignant tumor with high mortality, for which chemotherapy resistance is one of the main reasons. The high expression of ABCG2 in the cancer cells and expulsion of anticancer drugs directly cause multidrug resistance (MDR). Therefore, the development of new ABCG2 inhibitors that block the active causes of MDR may provide a strategy for the treatment of colorectal cancer. In this study, we find that dorsomorphin (also known as compound C or BML-275) potently inhibits the transporter activity of ABCG2, thereby preserving the chemotherapeutic agents mitoxantrone and doxorubicin to antagonize MDR in ABCG2-overexpressing colorectal cancer cells. Additionally, dorsomorphin does not alter ABCG2 protein expression. The results of molecular docking studies show that dorsomorphin is bound stably to the ABCG2-binding pocket, suggesting that dorsomorphin is a potent ABCG2 inhibitor that attenuates ABCG2-mediated MDR in colorectal cancer.

Robust compressed ghost imaging against environmental influence factors.

Ghost imaging based on sparse sampling is sensitive to the environmental influence factors frequently encountered in practice, such as instrumental drift and ambient light change, which could cause degradation of image quality. In this manuscript, we report a robust compressed sensing technique which could effectively reduce the influence of measurement errors on image quality. For demonstration purposes, we implement the proposed technique to ghost imaging, namely differential compressed sensing ghost imaging (DCSGI). By applying differential measurements n times, the first n Taylor expansion polynomials of the error could be eliminated in n-order DCSGI. It has been verified theoretically and experimentally that DCSGI works well with typical errors which exists in the realities of ghost imaging applications, while the conventional approach can hardly. In addition, the proposed technique may also replace conventional compressed sensing in other applications for anti-interference high-quality reconstruction.

Study of computational sensing using frequency-domain compression.

The computational sensing and imaging technique has been extended from spatial domain to temporal domain for capturing fast light signals with a slow photodetector. However, temporal computational sensing based on random source/modulation has to require a lot of measurements to reconstruct an object signal with acceptable SNR. In this paper, we study the frequency-domain acquisition technique for capturing a nanosecond temporal object with ten Hertz detection bandwidth. The frequency-domain acquisition technique offers a SNR gain of N, where N denotes the point number of Fourier spectrum. Because of the compressibility of data and the orthogonality and completeness of Fourier basis, it enables the reconstruction based on sub-Nyquist sampling. Because the slow detection only has low temporal resolution capability, the frequency-domain acquisition technique could provide robustness and is immune to the temporal distortion in experiments.

High Expression of Ten Eleven Translocation 1 Is Associated with Poor Prognosis in Hepatocellular Carcinoma.

Background: DNA methylation patterns have been found to be distinct between tumor and normal patients. However, the effect of DNA demethylation enzymes, ten eleven translocation (TET) proteins, has not been comprehensively characterized in liver cancer. In this research, we sought to unravel the linkage of TET proteins with prognosis, immune characteristics and biological pathways in hepatocellular carcinoma (HCC). Materials and Methods: Four independent datasets with gene expression data and clinical data of HCC samples were downloaded from public databases. CIBERSORT, single sample Gene Set Enrichment Analysis (ssGSEA), MCP-counter, and TIMER were implemented to evaluate immune cell infiltration. limma was employed to screen differentially expressed genes (DEGs) between two groups. The demethylation-related risk model was established by using univariate Cox regression analysis, the least absolute shrinkage and selection operator (LASSO), and stepwise Akaike information criterion (stepAIC). Results: TET1 was significantly higher expressed in tumor samples than that in normal samples. HCC patients with advanced stages (III+IV) and grades (G3+G4) had higher TET1 expression compared to early stages (I+II) and grades (G1+G2). HCC samples with high TET1 expression had worse prognosis than that with low expression. High and low TET1 expression groups had distinct immune cell infiltration and response to immunotherapy and chemotherapy. We identified 90 DEGs related to DNA demethylation in high vs. low TET1 expression groups. Furthermore, we established a risk model based on 90 DEGs containing seven key prognostic genes (SERPINH1, CDC20, HACD2, SPHK1, UGT2B15, SLC1A5, and CYP2C9) with effectiveness and robustness in predicting HCC prognosis. Conclusions: Our study suggested TET1 as a potential indicator in HCC progression. TET1 was closely involved in immune infiltration and activation of oncogenic pathways. The DNA demethylation-related risk model was potential to be applied for predicting HCC prognosis in clinics.

Application of the En Bloc Concept Combined with Anatomic Resection in Laparoscopic Hepatectomy.

Laparoscopic hepatectomy has been reported in many studies, and it is the mainstream method of liver resection. In some particular cases, such as when there are tumors adjacent to the cystic bed, surgeons cannot palpate the surgical margins through the laparoscopic approach, which leads to uncertainty about R0 resection. Conventionally, the gallbladder is resected first, and the hepatic lobes or segments are resected second. However, tumor tissues can be disseminated in the above cases. To address this issue, based on the recognition of the porta hepatis and intrahepatic anatomy, we propose a unique approach to hepatectomy combined with gallbladder resection by en bloc anatomic resection in situ. Firstly, after dissecting the cystic duct, without cutting the gallbladder primarily, the porta hepatis is pre-occluded by the single lumen ureter; secondly, the left hepatic pedicle is made free by the gap of the Laennec membrane and Hilar plate; thirdly, the assistant is asked to drag the fundus of the gallbladder, and the liver parenchyma tissue is resected using a harmonic scalpel along the ischemia line on the liver surface and intraoperative ultrasound. The whole middle hepatic vein (MHV) and its tributaries appear completely; lastly, the left hepatic vein (LHV) is disconnected, and the specimen is taken out from the abdominal cavity. The tumor, gallbladder, and other surrounding tissues are resected en bloc, which meets the tumor-free criterion, and a wide incisal margin and R0 resection are achieved. Therefore, the laparoscopic hepatectomy with the combination of the en bloc concept and anatomic resection is a safe, effective, and radical method with low postoperative recurrence and metastasis.

Long non-coding RNA HOXB-AS1 is a prognostic marker and promotes hepatocellular carcinoma cells' proliferation and invasion.

Long non-coding RNAs (lncRNAs) are broadly transcribed in the genome of human and play critical roles in the progression of multiple diseases. Long non-coding HOXB cluster antisense RNA 1 (HOXB-AS1) is a tumor exciter in various cancers. This study aimed to investigate the involvement of HOXB-AS1 in hepatocellular carcinoma (HCC). In the following study, HOXB-AS1 was unveiled to be highly expressed in HCC tissues as opposed to normal tissues. Silencing of HOXB-AS1 led to the loss of proliferation, migration, and invasiveness of HCC cells, namely Hep3B and Huh7. Moreover, the data showed that expression levels of HOXB-AS1 contribute significantly to the patient's survival rates. Otherwise, HOXB-AS1 levels in the serum of patients proved HOXB-AS1 as a biomarker for analysis and treatment of HCC. In summary, this study highlights HOXB-AS1 as key upregulated lncRNA in HCC which being an oncogene can cause proliferation and metastasis of HCC cells. The results also highlighted HOXB-AS1 as a promising biomarker for early diagnosis and prognosis of patients with HCC.

Application of Hemostatic Devices in Laparoscopic Hepatectomy.

Laparoscopic hepatectomy is considered a conventional method for treating benign and malignant liver diseases because it is a minimally invasive method. Despite its non-invasive aspect, bleeding and bile leakage occur in liver parenchyma tissue resection during the operation or in the post-operation period, indicating the requirement for high-grade hemostatic devices, such as ultrasonic surgical aspiration, bipolar electrocoagulation, etc. The lack of availability of these high-grade hemostatic devices prevents laparoscopic hepatectomy from becoming a generalized procedure in basic medical organizations. In view of the situation mentioned above, a suite of simple and easy hemostatic devices is developed in this protocol, which includes a harmonic scalpel, monopole electrocoagulation, and a single lumen catheter, to innovatively perform liver parenchyma tissue resection. First of all, the porta hepatis or hepatic pedicle is occluded intermittently by a single lumen catheter, followed by clamping for 15 min and releasing for 5 min. Subsequently, using the harmonic scalpel, clamping and crushing of the liver are done to cut off the hepatic parenchyma tissue and to reveal the intrahepatic arteries, veins, and bile ducts. Lastly, the bleeding spots are coagulated by using monopole electrocoagulation at each spot. Intrahepatic pipeline structures are then visible by using these methods, which could stop bleeding easily, reduce the incidence rate of bile leakage, and improve the safety and feasibility of laparoscopic hepatectomy. Therefore, the simple and easy hemostatic devices shown here are suitable for conducting procedures in primary medical institutions.

Tumor-associated macrophages promote cholangiocarcinoma progression via exosomal Circ_0020256.

This study investigated the exosomal circular RNAs (CircRNAs) produced by tumor-associated macrophages and delivered into the microenvironment of cholangiocarcinoma cells in order to use them as molecular targets for clinical therapy. Tumor-associated M2 macrophages (TAMs) were induced from THP-1 cells and identified by flow cytometry. The TAM-secreted exosomes were isolated from conditioned medium and a CircRNA microarray assay was performed to identify CircRNAs that were uniquely expressed in the isolated exosomes. Circ_0020256 was especially identified based on having the highest differential expression level among all of the CircRNA candidates. In vitro and in vivo experiments were performed to assess the effects of TAMs, exosomes, and Circ_0020256 on the growth and migration of cholangiocarcinoma (CCA) cells. The induced TAMs promoted the proliferation, migration, and invasion of CCA cells and those effects were mediated by exosomes secreted by the TAMs. In CCA cells (RBE and HCCC-9810), Circ_0020256 significantly promoted cellular activity by interacting with its intra-cellular microRNA target, miR-432-5p. In contrast, overexpression of transcription factor E2F3 in CCA cells restored the CCA cellular activities that were inhibited by miR-432-5p. On the other hand, treatment with small interference RNA (siRNA) for Circ_0020256 inhibited CCA cell proliferation, migration, and invasion both in vitro and in vivo. In conclusion, Circ_0020256 in TAM-secreted exosomes promoted the proliferation, migration, and invasion of CCA cells, and that promotional activity was regulated via a Circ_0020256/miR-432-5p/E2F3 axis.

Identification of resection plane for anatomical liver resection using ultrasonography-guided needle insertion.

Purposes: To set up an easy-handled and precise delineation of resection plane for hepatic anatomical resection (AR). Methods: Cases of AR using ultrasonography-guided needle insertion to trace the target hepatic vein for delineation of resection planes [new technique (NT) group, n = 22] were retrospectively compared with those without implementation of this surgical technique [traditional technique (TT) group, n = 29] in terms of perioperative courses and surgical outcomes. Results: The target hepatic vein was successfully exposed in all patients of the NT group, compared with a success rate of 79.3% in the TT group (P < 0.05). The average operation time and intraoperative blood loss were 280 ± 32 min and 550 ± 65 ml, respectively, in the NT group. No blood transfusion was required in either group. The postoperative morbidities (bile leakage and peritoneal effusion) were similar between groups. No mortality within 90 days was observed. Conclusions: Ultrasonography-guided needle insertion is a convenient, safe and efficient surgical approach to define a resection plane for conducting AR.

pH-responsive black phosphorus quantum dots for tumor-targeted photodynamic therapy.

Black phosphorus quantum dots(BPQDs) have shown a good application prospect in the field of tumor therapy due to their photoelectric effect and good biodegradability. Due to the active endocytosis and fast metabolic efficiency of tumor cells, BPQDs are easy to be absorbed by tumor cells. However, this does not guarantee that BPQDs will be completely targeted to tumor cells, and normal cells will also absorb BPQDs. Because the cell membrane is negatively charged, BPQDs are also negatively charged and are not easily absorbed by cells under the action of electrostatic repulsion. Surface pegylation is the most common modification method of black phosphorus at present. However, surface pegylation can reduce the uptake of BPQDs by tumor cells. Positive PEG is also easy to be recognized and swallowed by the reticuloendothelial system. The inherent instability and poor tumor targeting of BPQDs under physiological conditions limit further research and clinical application. For this purpose, we selected cationic polymer polyethylenimine (PEI) to modify BPQDs and then added RGD peptides targeting tumor cells. An outer layer of negatively charged PEG+DMMA makes the nanosystem more stable . In the acidic environment of the tumor, the PEG layer has a charge reversal, and the positively charged PEI and the RGD polypeptide BPQDs targeted by the tumor cells are released into the tumor cells. It provides a new method for efficiently and accurately transporting BPQDs, a novel photosensitive nanomaterial, into tumor cells for photodynamic therapy.

Photodynamic immunotherapy of cancers based on nanotechnology: recent advances and future challenges.

Photodynamic therapy (PDT) is a non-invasive or minimally-invasive treatment which applies photosensitizers (PSs) to create reactive oxygen species (ROS) exposed to light trigger to destroy cancer cells. PDT can activate host anti-tumor immune responses but not powerful enough to kill metastatic tumors. Because of its carrier advantage, imaging, and therapeutic function together with enhanced permeability and retention (EPR) effect, nano-materials have already been used in photo-immunotherapy. Herein, photodynamic immunotherapy (PDIT) based on nanotechnology seems to be a hopeful new form of cancer therapy. In this article, we firstly summarize the recent development in photodynamic immunotherapy based on nanotechnology.

Long-term results of ERCP- or PTCS-directed photodynamic therapy for unresectable hilar cholangiocarcinoma.

BACKGROUND: Photodynamic therapy (PDT) can be performed as palliative therapy for cholangiocarcinoma, while there is currently insufficient evidence for the efficacy. The aim of this study was to explore the clinical efficacy and safety of endoscopic retrograde cholangiopancreatography (ERCP)- or percutaneous transhepatic cholangioscopy (PTCS)-directed PDT combined with stent placement for unresectable hilar cholangiocarcinoma. METHODS: A retrospective analysis was conducted on 62 patients with unresectable hilar cholangiocarcinoma. Thirty patients received PDT using hematoporphyrin combined with biliary stent placement (PDT+stent group), including 22 receiving ERCP-directed PDT and 8 receiving PTCS-directed PDT. Survival time, quality of life, and postoperative adverse events were compared to 32 patients receiving biliary stent placement alone (Stent-only group). RESULTS: After 42 months of follow-up, median survival time was significantly longer in the PDT+stent group than the Stent-only group (14.2 vs. 9.8 months, P = 0.003). In the PDT+stent group, the median survival time was longer in the 6 patients with recurrence after surgical resection than the 24 patients without prior surgical resection (20.0 vs. 13.0 months, P = 0.017). The QOL total scores was significantly higher in the PDT+stent group than the Stent-only group at postoperative 6, 9, and 12 months (P<0.05). There was no significant difference in the incidence of postoperative adverse events between the two groups (24 [38.7%] vs. 20 [29.0%], P = 0.239). CONCLUSION: ERCP- or PTCS-directed PDT + stent placement can prolong the survival of patients with unresectable hilar cholangiocarcinoma, especially those with recurrence and improve quality of life without increasing adverse events.

Correction to: Exosomal miR-21 regulates the TETs/PTENp1/PTEN pathway to promote hepatocellular carcinoma growth.

Following the publication of article [1], the authors found that the images of Transwell Matrigel invasion (Fig. 7d) are incorrect.

Exosomal miR-21 regulates the TETs/PTENp1/PTEN pathway to promote hepatocellular carcinoma growth.

BACKGROUND: As an important means of communication, exosomes play an important role in the development of hepatocellular carcinoma (HCC). METHODS: Bioinformatics analysis, dual-luciferase reporter assays, methylation-specific quantitative PCR, and ChIP-PCR analysis were used to gain insight into the underlying mechanism of miR-21 in HCC. RESULTS: The detection of miRNAs in exosomes of HCC showed that miR-21 expression in exosomes was positively correlated with the expression level of miR-21 in cells and negatively correlated with the expression of its target genes PTEN, PTENp1 and TETs. HCC cell-derived exosomes could increase miR-21 and p-Akt expression in HCC cells and downregulate the expression of PTEN, PTENp1 and TETs. MiR-21 inhibitors or PTENp1 overexpression vectors could weaken the effect of the abovementioned exosomes and simultaneously weaken their role in promoting cell proliferation and migration and inhibiting apoptosis. Further studies showed that miR-21 not only directly regulated the expression of PTEN, PTENp1 and TETs but also increased the methylation level of the PTENp1 promoter by regulating the expression of TETs, thereby inhibiting the expression of PTENp1 and further downregulating the expression of PTEN. CONCLUSIONS: Exosomal miR-21 can regulate the expression of the tumor suppressor genes PTEN and PTENp1 in various ways and affect the growth of HCC cells.

Long noncoding RNA LINC01296 promotes tumor growth and progression by sponging miR-5095 in human cholangiocarcinoma.

The aim of the present study was to elucidate whether, and how, long intergenic non-protein coding RNA 1296 (LINC01296) is involved in the modulation of human cholangiocarcinoma (CCA) development and progression. Microarray data analysis and reverse transcription-quantitative polymerase chain reaction analysis demonstrated that LINC01296 was significantly upregulated in human CCA compared with nontumor tissues. Furthermore, the expression of LINC01296 in human CCA was positively associated with tumor severity and clinical stage. Knockdown of LINC01296 dramatically suppressed the viability, migration and invasion of RBE and CCLP1 cells, and promoted cell apoptosis in vitro. Furthermore, LINC01296 knockdown inhibited tumor growth in a xenograft model. Mechanistically, LINC01296 was demonstrated to sponge microRNA-5095 (miR-5095), which targets MYCN proto-oncogene bHLH transcription factor (MYCN) mRNA in human CCA. By inhibition of miR-5095, LINC01296 overexpression upregulated the expression of MYCN and promoted cell viability, migration and invasion in CCA cells. The results reveal that the axis of LINC01296/miR-5095/MYCN may be a mechanism to regulate CCA development and progression.

Role of AP-2α and MAPK7 in the regulation of autocrine TGF-ß/miR-200b signals to maintain epithelial-mesenchymal transition in cholangiocarcinoma.

BACKGROUND: Cholangiocarcinoma (CCA) is characterized by early lymphatic, metastasis, and low survival rate. Epithelial-mesenchymal transition (EMT) is able to induce tumor metastasis. Although the TGF-ß/miR-200 signals promote EMT in various types of cancer, the regulatory mechanism in CCA is still unclear. METHODS: Expression of miR-200b, TGF-ß, and EMT markers were measured in tumor samples and cell lines by qRT-PCR and western blot. CCK8 assay was performed to measure the cell viability. Transwell assay was used to evaluate migration and invasion. The target genes of miR-200b and transcription factor of TGF-ß were analyzed using dual-luciferase reporter system. RESULTS: We have demonstrated that CCA exhibited remarkable EMT phenotype and miR-200b was reduced in CCA patients (n = 20) and negatively correlated to TGF-ß. Moreover, two CCA cells, HCCC, and RBE, with epithelial appearances treated with TGF-ß, showed fibroblastic-like cell morphology with downregulated miR-200b expression. Forced expression of miR-200b abrogated TGF-ß-induced EMT initiation, with decreased cell proliferation, migration, and invasion in vitro. Also, TFAP2A (encode AP-2α) and MAPK7 were found to be targeted by miR-200b to downregulate EMT and AP-2α inhibited miR-200b by directly promoting transcription of TGFB1. Overexpression of MAPK7 significantly reversed miR-200b-induced inhibition of EMT, migration, and proliferation by increasing the expression of TGF-ß, cyclin D1, and Cdk2. Further, the administration of miR-200b induced a remarkably tumor regression in vivo and reduced the effect of TGF-ß-related EMT in AP-2α and MAPK7-dependent manner. CONCLUSIONS: Our study highlights that miR-200b-based gene therapy is effective in the treatment of CCA.

Peroxisome proliferator-activated receptor-γ inhibits pancreatic cancer cell invasion and metastasis via regulating MMP-2 expression through PTEN.

The invasive and metastatic behavior of pancreatic cancer is associated with a poor prognosis. Therefore, understanding the molecular mechanisms underlying the invasion and metastasis of pancreatic cancer has important application values theoretically and clinically. In previous years, with increasing studies focusing on tumor pathogenesis, it has been revealed that peroxisome proliferator­activated receptor­Î³ (PPARγ) and phosphatase and tensin homolog (PTEN) are closely associated with the occurrence and development of pancreatic cancer. Thus, in the present study, a scratch wound assay, western blotting and transwell assays were used to investigate their function. The scratch wound assay demonstrated that treatment with the PPARγ ligand rosiglitazone (RGZ) could reduce the movement and migration of pancreatic cancer cells. Western blotting results indicated that while RGZ inhibited the expression of matrix metalloproteinase (MMP)­2, PPARγ inhibitors promoted MMP­2 expression. However, PPARγ ligands and inhibitors did not affect the expression of MMP­9. Further investigation indicated that the regulation of MMP­2 by PPARγ activation occurred through PTEN. In addition, PPARγ activation promoted PTEN expression, thereby inhibiting the expression of MMP­2. Subsequent transwell experiments demonstrated that RGZ treatment significantly inhibited the invasiveness of pancreatic cancer cells and the inhibitory effect of RGZ was completely reversed by simultaneous transfection of the MMP­2­overexpressing vector, which increased the invasiveness of pancreatic cancer cells. Therefore, PPARγ activation can activate PTEN expression, thereby suppressing the expression of MMP­2 and hence inhibiting the invasion and metastasis of pancreatic cancer cells.

MiR-324-5p Suppresses Hepatocellular Carcinoma Cell Invasion by Counteracting ECM Degradation through Post-Transcriptionally Downregulating ETS1 and SP1.

Hepatocellular carcinoma (HCC) is one of the common malignancies, which is highly metastatic and the third common cause of cancer deaths in the world. The invasion and metastasis of cancer cells is a multistep and complex process which is mainly initiated by extracellular matrix (ECM) degradation. Aberrant expression of microRNA has been investigated in HCC and shown to play essential roles during HCC progression. In the present study, we found that microRNA-324-5p (miR-324-5p) was downregulated in both HCC cell lines and tissues. Ectopic miR-324-5p led to the reduction of HCC cells invasive and metastatic capacity, whereas inhibition of miR-324-5p promoted the invasion of HCC cells. Matrix metalloproteinase 2 (MMP2) and MMP9, the major regulators of ECM degradation, were found to be downregulated by ectopic miR-324-5p, while upregulated by miR-324-5p inhibitor. E26 transformation-specific 1 (ETS1) and Specificity protein 1 (SP1), both of which could modulate MMP2 and MMP9 expression and activity, were presented as the direct targets of and downregulated by miR-324-5p. Downregulation of ETS1 and SP1 mediated the inhibitory function of miR-324-5p on HCC migration and invasion. Our study demonstrates that miR-324-5p suppresses hepatocellular carcinoma cell invasion and might provide new clues to invasive HCC therapy.

Activation of peroxisome proliferator-activated receptor-γ (PPARγ) inhibits hepatoma cell growth via downregulation of SEPT2 expression.

Hepatocellular carcinoma (HCC) is a malignant tumor with poor prognosis and low therapeutic efficacy. Recent studies have demonstrated the therapeutic prospect of peroxisome proliferator-activated receptor-γ (PPARγ) cancer angiogenesis. However, the action mechanisms remain elusive. In the present study, by using mass spectrometry, we found that PPARγ ligand rosiglitazone (RGZ) could regulate HCC cell growth by influencing various downstream factors and pathways. Among the altered proteins, septin 2 (SEPT2) was found to exhibit oncogenic function. PPARγ overexpression could inhibit the expression of SEPT2, thus blocking the promoting effects of SEPT2 on HCC cell proliferation, invasion and its inhibitory effect on cell apoptosis. Further studies also indicated that SEPT2 promoted HCC cell growth via upregulation of matrix metalloproteinase (MMP)-2 and -9, and simultaneously inhibited the cleavage of caspase-3, -7, and -9. Interestingly, the effects of SEPT2 on the above factors could be suppressed by PPARγ overexpression, suggesting that PPARγ could inhibit HCC cell growth via regulating the expression and blocking the oncogenic function of SEPT2. Taken together, these results provide new evidence for the action mechanisms of PPARγ in carcinogenesis of HCC, and upon further investigation, PPARγ could be developed as a new target for the treatment of liver cancer.