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Background To investigate the expression and diagnostic value of seven autoantibodies (P53, PGP9.5, SOX2, GAGE7, GBU4-5, MAGE, and CACE) in lung cancer patients. Methods A total of 370 patients were admitted to the Thoracic Surgery of the First Affiliated Hospital of Suzhou University from 2017 to 2019, including 305 patients with lung cancer and 65 patients with benign lesions. The concentrations of the seven autoantibodies were determined by enzyme linked immunosorbent assay (ELISA).The expression levels of each antibody were compared between the two groups, and the levels of each antibody between lung cancer patients with different pathological types were also compared. We aimed to analyze the diagnostic efficiency of single antibody detection combined with seven antibodies, and also to explore whether there were differences among the positive rates of each antibody in sex, age, smoking history, pathological classification, and clinical stages in the lung cancer group. Results The expression levels of seven autoantibodies in the lung cancer group were higher than those in the benign lesion group. In the lung cancer group, the expression levels of the seven autoantibodies did not vary statistically among different pathological types. The area under the curve of combined detection of the seven antibodies reached 0.735, and the Y-index reached 0.35, which was higher than that of single antibody detection. P53 exhibited the highest sensitivity and lowest specificity; meanwhile, PGP9.5, SOX2, GAGE7, GBU4-5, and MAGEA1 exhibited low sensitivity and high specificity. The sensitivity and specificity of the CAGE were approximately 60%, respectively. There was no statistical difference in the positive rate of each antibody in age, smoking history, and clinical stage. The positive rate of MAGEA1 and CAGE was statistically different in sex, and the positive rate of MAGEA1 was statistically different in pathological classification. Conclusions The seven autoantibodies of lung cancer can potentially be used as an auxiliary examination method for the early diagnosis of lung cancer.

Background EC (esophageal cancer) is a common cancer among people in the world. The molecular mechanism of FAM196B (family with sequence similarity 196 member B) in EC is still unclear. This article aimed to clarify the role of FAM196B in EC. Methods The expression of FAM196B in EC tissues was detected using qRT-PCR. The prognosis of FAM196B in EC patients was determined by log-rank kaplan-Meier survival analysis and Cox regression analysis. Furthermore, shRNA was used to knockdown the expression of FAM196B in EC cell lines. MTT, wound healing assays and western blot were used to determine the role of FAM196B in EC cells. Results In our research, we found that the expression of FAM196B was up-regulated in EC tissues. The increased expression of FAM196B was significantly correlated with differentiation, lymph node metastasis, stage, and poor survival. The proliferation and migration of EC cells were inhibited after FAM196B-shRNA transfection in vitro and vivo. The western blot result showed that FAM196B could regulate EMT. Conclusion These results suggested that FAM196B severs as an oncogene and promotes cell proliferation and migration in EC. In addition, FAM196B may be a potential therapeutic target for EC patients.

Background: Adenoid cystic carcinoma (ACC) refers to a salivary gland neoplasm. Tracheal adenoid cystic carcinoma that invades the tracheal prominence is a relatively rare tumor among thoracic diseases. Objective: To explore the epidemiology, diagnosis, treatment and future development of tracheal adenoid cystic carcinoma (TACC). Methods: With asymptomatic invasion of the tracheal prominence, a case of tracheal adenoid cystic carcinoma with asymptomatic invasion of the tracheal prominence was reported. The clinical management process and surgical methods were introduced, and related literature was reviewed and summarized. Results: The patient was admitted due to tracheal augmentation mass for half a month. Chest CT at admission displayed the soft tissue density shadow behind the tracheal augmentation process. After the completion of other examinations, tracheal tumor resection and tracheal reconstruction were performed. Postoperative routine pathology exhibited that it was TACC and without inguinal lymph node metastasis. Conclusion: TACC is a low-grade tracheal tumor with low incidence, delayed clinical manifestations and lack of specificity as well. CT and bronchoscopy are helpful for the diagnosis of suspected patients. Meanwhile, radical surgical resection is the first choice of treatment. Adjuvant therapy can improve the therapeutic effect. Targeted immunotherapy is the developing direction of treatment.

The Insulin-like growth factor-1/Insulin-like growth factor-1 receptor (IGF1/IGF1R) axis contributes to immunosuppression during tumor progression; however, the underlying mechanism remains unclear. In the present study, we found that IGF1 stimulation or IGF1R overexpression (IGF1R-OE) could upregulate the expression of B7-H4, while IGF1R inhibition downregulated B7-H4 in both A549 and SPC-A-1 lung cancer cell lines. IGF1R-OE conferred the inhibition of CD8+ T cells by cancer cells in vitro, and induction of B7-H4 expression was mediated by the activation of the MEK/ERK1/2 signaling pathway. The in vitro findings were further confirmed in vivo using a Lewis lung cancer mouse model. IGF1R-OE promoted tumor growth and inhibited tumor infiltration by CD8+ T cells in the mouse model. However, this effect was suppressed when B7-H4 was knocked down in IGF1R-OE cells. Our findings suggest that IGF1R could induce immunosuppression in lung cancer by upregulating the expression of B7-H4 through the MEK/ERK pathway. B7-H4 may therefore be a potential therapeutic target for lung cancer immunotherapy.

OBJECTIVE To explore the safety and feasibility of thoracoscopic surgery in patients with lung cancer under non-intubation anesthesia, and to evaluate the advantages of the non-intubation anesthesia compared with intubation anesthesia on enhanced recovery after surgery (ERAS). METHODS A retrospective cohort study was conducted in which 100 patients who underwent thoracoscopic lung cancer surgery from January 2020 to February 2021 in the Department of Thoracic Surgery of the First Affiliated Hospital of Soochow University were included and divided into non-intubation group (n = 50) and intubation group (n = 50). The primary outcome was the comparison of intra- and postoperative parameters. Secondary outcomes included inflammatory response indicators and intra- and postoperative complications. RESULTS There was no significant difference between the two groups in anesthesia effect score, blood loss, lowest pulse oxygen saturation, operation time, postoperative chest tube indwelling time (P > 0.05). Non-intubation group had less intraoperative remifentanil dosage, less change of blood pressure and heart rate, lower postoperative pain numerical score(NRS), less medical costs, smaller incidence rate of throat discomfort (P

Background The comparison between relatively intact nanoscale extracellular vesicle-derived DNA (nEV-DNA) and fragmented circulating cell-free DNA (cfDNA) in mutation detection among patients with non-small-cell lung cancer (NSCLC) has not been carried out yet, and thus deserves investigation. Patients and methods Both nEV-DNA and cfDNA was obtained from 377 NSCLC patients with known EGFR mutation status and 69 controls. The respective EGFRE19del/T790M/L858R mutation status was interrogated with amplification-refractory-mutation-system-based PCR assays (ARMS-PCR). Results Neither nEV-DNA nor cfDNA levels show a strong correlation with tumor volumes. There is no correlation between cfDNA and nEV-DNA levels either. The detection sensitivity of nEV-DNA and cfDNA using ARMS-PCR in early-stage NSCLC was 25.7% and 14.2%, respectively, with 96.6% and 91.7% specificity, respectively. In late-stage NSCLC, both nEV-DNA and cfDNA show ∼80% sensitivity and over 95% specificity. Conclusions nEV-DNA is superior to cfDNA for mutation detection in early-stage NSCLC using ARMS-PCR. However, the advantages vanish in late-stage NSCLC.

Background This study aimed to investigate the relationship between RNA polymerase II subunit 5 (RPB5)-mediating protein (RMP) and clinicopathological characteristics of non-small cell lung cancer (NSCLC) patients by measuring the expression level of RMP in human NSCLC tissues and cell lines. At the same time, we studied the impact of RMP on the biological function of cancer, providing strong support for gene targeted therapy of NSCLC. Methods Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were used to determine the expression levels of messenger (m)RNA and protein in NSCLC cell lines and tissues. Cell counting kit 8 (CCK8) assay and flow cytometry were selected to detect cell proliferation, cycle and apoptosis. The wound healing assay was chosen to detect the migration and invasion ability of cells. The xenograft model was performed to study the function of RMP in vivo. Immunohistochemical (IHC) staining showed the levels of RMP, Bcl-2, Bax and caspase-3. Results First, mRNA and protein levels of RMP were relatively overexpressed in NSCLC cells. Compared with the corresponding normal tissues, the mRNA and protein levels of RMP were significantly higher in human NSCLC tissues. Concurrently, we found that the expression of RMP was related to the status of lymph nodes (LNs) in cancer tissues and T stage. Then, RMP overexpression promoted the proliferation of A549. At the same time, RMP provided A549 cells the ability to resist chemotherapy and radiotherapy; when A549 cells were treated with gefitinib and radiation, RMP reduced apoptosis. We also found that RMP can protect A549 from G2 block caused by radiation. Over-irradiated RMP-overexpressed A549 cells had lower Bcl2-associated X protein (Bax) levels and higher B-cell lymphoma 2 (Bcl-2) levels. The migration and invasion ability of A549 cells was increased by RMP. Finally, RMP can promote tumor growth by increasing Bcl-2 levels and decreasing Bax and caspase-3 levels in the xenograft model. Conclusions There is potential for RMP to develop into a diagnostic and therapeutic target for NSCLC.

Background This study investigated the clinical efficiency of enhanced recovery after surgery (ERAS) using uniportal video-assisted thoracoscopic surgery for lung cancer. Methods The clinical data of 83 patients with early-stage non-small cell lung cancer (NSCLC) at the First Affiliated Hospital of Soochow University from January 2016 to February 2017 were retrospectively analyzed. ERAS was applied to 38 patients (ERAS group), while 45 patients received conventional surgical treatment (control group). The operative duration, number of lymph nodes retrieved, blood loss, visual analogue scale (VAS), postoperative duration of chest tube placement, length of hospital stay, and postoperative complications were compared between the groups. Results Surgeries were conducted successfully in all patients, and no mortality occurred during the perioperative period. The ERAS group had better VAS on the third postoperative day, shorter chest tube duration, and shorter length of hospital stay (P 0.05). Conclusions ERAS using uniportal video-assisted thoracoscopic surgery for NSCLC patients is safe and practicable, and could also reduce the length of hospital stay.

e21067 Background: Efficacy of BRCA1/2 inhibitor in non-small cell lung cancer (NSCLC) is under investigation in serval clinical trials. Meanwhile immune checkpoint inhibitor (ICI) has become one of the standard therapies for advanced NSCLC, while its efficacy in BRCA mutant NSCLC is not clear. This study assessed the efficacy of anti-PD-(L)1/CTLA-4 in advanced BRCA-mutant NSCLC. Methods: Data of cohort OAK, POPLAR and Rizvi et al.,2018 was downloaded. Efficacy including objective response rate (ORR), progression-free survival (PFS) and overall survival (OS) were reviewed for BRCA1/2 mutant and wild-type group. The impact of mutant gene ( BRCA1, BRCA2), histological types (adenocarcinoma, squamous) and tumor mutation burden ranges (TMB, > 10 SNVs/Mb, < 10 SNVs/Mb) was analyzed if information was available. Results: A total of 809 ICI-treated advanced NSCLC patients, including 53 (6.6%) with BRCA1/2 mutation, were identified. In OAK/POPLAR cohort (atezolizumab monotherapy, 2nd line or more), TMB in BRCA1/2 mutant group was significant higher (19.2 vs. 10.24, P=0.008) than group of wild-type. The ORR of mutant group was 21.9% (Table), median PFS was 2.5 months, median OS was 9.5 months. The ORR and PFS were comparable between mutant and wild-type groups, while OS of the mutant group was significantly shorter than that in wild-type group (mOS, 9.5 months vs. 14.1 months, P= 0.02). Within mutant group, no significant difference of ORR, PFS and OS were found between mutant gene ( BRCA1 vs. BRCA2), histological type (adenocarcinoma vs. squamous) and TMB range (>10 vs. st line or more), TMB in mutant group was also significant higher (22.2 vs. 9.1, P=0.04) than wild-type group. ORR, PFS for mutant and wild-type groups were 25.0% vs. 20.1%, 3.2 months vs. 3.4 months, without significant difference. Within mutant group, superior PFS was found in adenocarcinoma subgroup (mPFS, 5.5 months vs. 1.2 months (squamous subgroup), P = 0.008) and BRCA2-mutant subgroup tend to have superior PFS (mPFS 5.5 months vs. 1.8 months, P=0.08) than BRCA1-mutant subgroup. Conclusions: This retrospective multicohort analysis showed a trend of worse survival in BRAC-mutant NSCLC patients after ICI treatment compared to those in wild-type group, in spite of higher TMB level. Analysis with more samples are needed to provide more precise treatment reference. [Table: see text]

The prognostic role of programmed cell death-ligand 1 (PD-L1) in non-small cell lung cancer (NSCLC) remains controversial. This meta-analysis was conducted to clarify the association of PD-L1 with survival in NSCLC patients.Relevant studies were collected from PubMed, Embase and Web of Science. Only studies in which PD-L1 expression was detected by immunohistochemical staining in NSCLC patients correlated with patient survival data were included. Stata 12.0 was performed in this meta-analysis.Fifteen studies with 3116 patients were included in this meta-analysis. The combined hazard ratio (HR) of 1.18 (95%CI, 0.90-1.56; P0.05) shows that PD-L1 over-expression in NSCLC patients didn't associate with overall survival (OS). However, subgroup analysis indicated that PD-L1 over-expression was correlated with poor OS in Asian patients (HR=1.84, 95%CI: 1.14-2.28; P0.001). Moreover, the results suggested that a significant relationship between PD-L1 expression and OS was also showed in studies with late stage (HR=1.27, 95%CI: 1.06-1.48; P=0.031), poor tumor differentiation (HR=1.86, 95%CI: 1.35-2.64; P=0.001) and anaplastic lymphoma kinase (ALK) translocation (HR=2.58, 95%CI: 1.03-5.78; P=0.028).PD-L1 over-expression is correlated with a poor prognosis in Asian NSCLC patients.

The prognostic value of vascular endothelial growth factor C (VEGF-C) in patients with esophageal cancer (EC) remains controversial. The aim of this meta-analysis was to clarify the association of VEGF-C with survival in EC patients.We performed a meta-analysis that included eligible studies to expound the effect of VEGF-C in EC survival. Eligible studies published until November 2015 was identified using available databases. STATA 12.0 was performed in this meta-analysis.We identified 13 studies, including 1203 patients, in this meta-analysis. The combined hazard ratio of 1.70 (95% CI, 1.43-2.03, P0.001) shows that VEGF-C overexpression was significantly correlated with poor overall survival in EC patients. Furthermore, the results suggested a significant relationship between VEGF-C expression and overall survival was also showed in studies with patient source, patient number ≥ 70, methods detecting VEGF-C by reverse transcription PCR (RT-PCR) or ELISA and histology type. Moreover, combined odds ratio of VEGF-C displayed that VEGF-C overexpression was significantly association with stage, depth of tumor invasion, lymph node status and metastasis of EC (P0.05). However, it has no correlation with differentiation degree of EC (P0.05).VEGF-C overexpression shows an unfavorable prognosis for EC patients.

The prognostic role of survivin in esophageal cancer (EC) remains controversial. This meta-analysis aimed to clarify the association of survivin with survival in EC patients.Relevant studies published up to November 2014 were identified using PubMed and Embase. Only studies in which survivin was detected through immunohistochemical staining were included. STATA 12.0 was used in this meta-analysis.A total of 9 studies, which comprised 610 patients, were included in the meta-analysis. The combined hazard ratio (HR) of 1.76 (95% CI, 1.40-2.21; P0.001) suggests that survivin overexpression in EC patients was significantly associated with poor overall survival. Moreover, the results showed a significant relationship between overall survival and survivin expression was also displayed in studies with a non-Asian country (HR, 1.75; 95% CI, 1.30-2.35), patient number ≥ 50 (HR, 1.86; 95% CI, 1.57-2.20), the cut-off level ≥ 5% (HR, 1.43; 95% CI, 0.94-2.17) and the esophageal squamous cell carcinoma (HR, 1.82; 95% CI, 1.43-2.30). However, combined odds ratio of survivin indicated that survivin overexpression has no correlation with stage, grade of differentiation, lymph node status, depth of invasion and distant metastasis of EC (P0.05).Survivin overexpression is associated with poor prognosis in EC patients.

The smallest gene HBx of Hepatitis B virus (HBV) is recognized as an important viral oncogene (V-oncogene) in the hepatocarcinogenesis. Our previous work demonstrated that RMP is a cellular oncogene (C-oncogene) required for the proliferation of hepatocellular carcinoma (HCC) cells. Here we presented the collaboration between V-oncogene HBx and C-oncogene RMP in the development of HCC. The coexpression of HBx and RMP resulted in the cooperative effect of antiapoptosis and proliferation of HCC cells. In vivo, overexpression of RMP accelerated the growth of HBx-induced xenograft tumors in nude mice and vice versa HBx promoted the growth of RMP-driven xenograft tumors. Although HBx didn't regulate the expression of RMP, HBx and RMP interact with each other and collocalized in the cytoplasm of HCC cells. HBx and RMP collaboratively inhibited the expression of apoptotic factors and promoted the expression of antiapoptotic factors. This finding suggests that HBV may induce, or at least partially contributes to the carcinogenesis of HCC, through its V-oncoprotein HBx interacting with the C-oncoprotein RMP.

The aim of the present study was to address the effects of heat shock protein B6 (HspB6) on tumor growth and metastasis in BALB/c mice. Lewis lung carcinoma (LLC) cells were subcutaneously injected into BALB/c mice followed by intraperitoneal injection of recombinant HspB6 (HspB6 groups) or phosphate‑buffered saline (control groups). Tumor growth and metastasis were assessed by size measurement and weighing of tumors and cervical lymph nodes, respectively. Chemokine expression in tumor masses was quantified quantitative polymerase chain reaction and western blotting. Tumor cell apoptosis was detected by flow cytometric analysis. The proliferation and migration of LLC cells, stimulated with HspB6, were detected using Cell Counting Kit 8 and wound scratch assays in vitro. Tumors grafted into the BALB/c mice and intraperitoneally injected with HspB6 were significantly bigger in size than those grafted into the control mice. From 7 days following the injection, the weight of cervical lymph nodes in HspB6 groups was higher than that in the control mice. We also revealed that the apoptotic cell number in tumor masses in the HspB6 groups was lower than that of the control mice. CD31 expression of vascular endothelial cells was higher in tumors grafted in HspB6 groups than those grafted in the control mice. Concomitantly, the tumor tissue mRNA and protein expression enhancement of vascular endothelial growth factor, basic fibroblast growth factor and intercellular adhesion molecule 1 were greater in HspB6 mice than in the control mice. HspB6 also inhibited cell apoptosis and enhanced the migration and proliferation of LLCs in vitro. In conclusion, HspB6 exhibited tumor promotion through increasing tumor angiogenesis, tumor metastasis and inhibiting tumor cell apoptosis.

PDRG1, is short for P53 and DNA damage-regulated gene, which have been found over 10 years. Although severe studies have described the roles of PDRG1 separately in many kinds of tumors, how to act as an oncogene are unclear. To better verify the function of PDRG1 in lung cancer, both loss-function and gain-function of PDRG1 studies based on two human lung cancer lines were performed. Following the transfection of PDRG1, both A549 and 95-D cells showed significant changes in cell viability, the expression of some protein and apoptosis, which were all implied the PDRG1 is an oncogene. Another interesting finding is PDRG1 could promote radioresistance involved the ATM-p53 signaling pathway in lung cancer. If we combine radiotherapy with gene-targeted therapy together effectively, predominant effect may be acquired, which is a huge milestone in clinical cure about lung cancer.

The involvement of miR-96 in esophageal cancer (EC) remains unclear. The aim of this study is to explore the functional role of miR-96 and determine whether miR-96 could be a potential therapeutic target for human esophageal cancer. MiR-96 up-regulation was demonstrated in 145 EC samples and RECK down-regulation was validated in EC cell lines. Moreover, ectopic overexpression of miR-96 in TE-1 or ECa-109 contributed to tumor growth in xenograft mouse models. Furthermore, up-regulation of miR-96 could reduce the susceptibilities of EC cells to chemotherapy or radiotherapy. RECK was identified as a target of miR-96 and RECK overexpressing could abrogate the growth of EC cells induced by miR-96. Taken together, miR-96 serves as an oncogene role in EC cells through downregulating RECK.

This study was conducted to compare the perioperative outcomes of two-portal and three-port video-assist thoracoscopic surgery (VATS) for early stage nonsmall cell lung cancer.In this retrospective analysis, 279 cases of two-port VATS with a single utility port and 152 cases of three-port VATS performed by our department from October 2010 to December 2014 were collected. The operative time, volume of intraoperative blood loss, number of dissected lymph nodes, volume of postoperative pleural drainage, postoperative extubation time, and duration of postoperative hospitalization were compared between these 2 groups.No statistically significant differences on the operative time, volume of postoperative bleed, and the number of dissected lymph nodes was noted between two-port and three-port video-assist thoracoscopic surgery. Less postoperative pleural drainage, shorter extubation time, and postoperative hospitalization were observed in the two-port VATS group when compared with those of three-port VTAS groupTwo-port VATS decreased operative postoperative pleural drainage and resulted in shorter extubation time and postoperative hospitalization compared with three-port VATS. Two-port VATS is a safe and feasible approach for early stage nonsmall cell lung cancer.

SWI/SNF chromatin remodeling complexes are frequently mutated in a variety of human cancers. We investigated the mutation incidence and the role of mSWI/SNF (BAF) complexes in human lung cancer. In the present study, we analyzed somatic mutations of BAF complexes and other driver mutated genes of lung carcinoma deposited in the Catalogue of Somatic Mutations in Cancer (COSMIC) database. BAF complexes were mutated in 282 of 803 (35.12%) lung carcinoma samples analyzed, ranking second to TP53. Significantly, BAF-mutated samples exhibited more genomic mutations than BAF wild-type ones. Moreover, a significant positive correlation existed between the BAF mutations and overall genomic mutations in these lung carcinoma samples (P

MicroRNAs are emerging as a class of small regulatory RNAs whose specific roles and significant functions in the majority of carcinomas have yet to be entirely illustrated. The aim of this study is to explore the effect of miR-95 and determine whether miR-95 could be a potential therapeutic target for human non-small cell lung cancer. First of all, our study showed that miR-95 was highly expressed in both NSCLC cell lines (compared with normal cells) and tumor tissues (compared with corresponding normal tissues), whereas the protein level of SNX1 was downregulated in NSCLC cell lines. Next, we found that ectopic overexpression of miR-95 in A549 or H226 contributed to tumor growth in xenograft mouse models. In addition, the results also indicated that upregulation of miR-95 could significantly enhance the susceptibilities of NSCLC cells to chemo- or radiotherapy. Furthermore, using the luciferase reporter, we demonstrated that SNX1 is a direct target of miR-95. Meanwhile, overexpression of SNX1 could abrogate the growth of NSCLC cells induced by miR-95. Taken together, these results suggest that miR-95 functions as an oncogene role in NSCLC cells by directly targeting SNX1.

Background As a key element in the T-helper 17 (Th17) cell-mediated inflammatory process, interleukin-23 receptor (IL-23R) plays a crucial role in the pathogenesis of cancer. Single nucleotide polymorphisms (SNPs) in IL-23R have been frequently studied in several previous case-control cancer studies, but its association with esophageal squamous cell carcinoma (ESCC) in Chinese population has not been investigated. This study examined whether genetic polymorphisms in IL-23R were associated with ESCC susceptibility. Methods A hospital-based case-control study of 684 ESCC patients and 1064 healthy controls was performed to assess the association between four previous reported IL-23R genotypes (rs6682925, rs6683039, rs1884444 and rs10889677) and ESCC risk. The results revealed that the C allele of the rs10889677A>C polymorphism in the 3′UTR of IL-23R gene was inversely associated with the risk of ESCC. Results The rs10889677AC genotype had significantly decreased cancer risk (odds ratio [OR] = 0.85, 95% confidence interval [CI] = 0.69–1.01) compared to subjects homozygous carriers of rs10889677AA, the risk decreased even further in those carrying rs10889677CC genotype (OR = 0.64, 95% CI = 0.44–0.93). No significant association was found between the other three polymorphisms and the risk of ESCC. Conclusion These findings indicated that rs10889677A>C polymorphism in IL-23R may play a protective role in mediating the risk of ESCC.

RMP has been shown to function in the transcription regulation through association with RNA polymerase (RNAP) II subunit RPB5. It also has been shown to be required for the proliferation of hepatocellular carcinoma (HCC) cells with an antiapoptotic property. In this article, we further demonstrate that RMP displays distinct features in HCC cells compared with normal hepatic cells. RMP expression is remarkably increased in various cancer cell lines including HCC cells when compared with normal cells. Depletion of RMP could inhibit the proliferation of HCC cells, but not the normal hepatic cells. RMP significantly prevented apoptosis of HCC cells in SMMC-7721 and HepG2, but had little effect on apoptosis in the normal hepatic cells. The mechanisms of RMP's distinct features rely on different responsive expressions of apoptosis factors induced by RMP in HCC and hepatic cells. Either overexpression or depletion of RMP significantly affected the expression of apoptosis factors in HCC cells. However, normal hepatic cells showed a tendency to resist RMP for the regulation of apoptosis. In the clinical samples, the increased expression of RMP in HCCs was also observed when compared with the matched non-tumor tissues from 30 HCC patients. The different expression levels of and distinct responses to RMP between HCC and hepatic cells suggest that RMP might serve as not only a biomarker for the diagnosis of HCC, but also a potential target for the HCC therapy.