EEF1D stabilized by SRSF9 promotes colorectal cancer via enhancing the proliferation and metastasis.

Colorectal cancer (CRC) is the third most common cancer and causes high mortality worldwide. Although CRC has been studied widely, the molecular mechanism is not completely known. Eukaryotic translation elongation factor 1 delta (EEF1D) participates in the progression of various tumors, however, the effect of EEF1D on CRC remains unclear. Here, we aimed to identify the potential mechanism of EEF1D in CRC. The expression levels of EEF1D were assessed in CRC samples. Functional analysis of EEF1D in CRC was detected in vitro and in vivo. The regulatory mechanism of EEF1D was identified with RNA immunoprecipitation, RNA pull-down assay, and proteomics analysis. Our findings confirmed that EEF1D was upregulated in human CRC tissues. Functionally, EEF1D overexpression accelerated cell proliferation and metastasis, whereas EEF1D knockdown inhibited cell proliferation and metastasis both in vitro and in vivo CRC models. Furthermore, we showed that EEF1D was upregulated by SRSF9 via binding to 3'UTR of EEF1D mRNA. EEF1D knockdown reversed the malignant phenotype induced by SRSF9 overexpression. These findings demonstrated that EEF1D promotes CRC progression, and EEF1D may be a molecular target against CRC.

Cancer spreading patterns based on epithelial-mesenchymal plasticity.

Introduction: Metastasis is a major cause of cancer-related deaths, underscoring the necessity to discern the rules and patterns of cancer cell spreading. Epithelial-mesenchymal plasticity contributes to cancer aggressiveness and metastasis. Despite establishing key determinants of cancer aggressiveness and metastatic ability, a comprehensive understanding of the underlying mechanism is unknown. We aimed to propose a classification system for cancer cells based on epithelial-mesenchymal plasticity, focusing on hysteresis of the epithelial-mesenchymal transition and the hybrid epithelial/mesenchymal phenotype. Methods: We extensively reviewed the concept of epithelial-mesenchymal plasticity, specifically considering the hysteresis of the epithelial-mesenchymal transition and the hybrid epithelial/mesenchymal phenotype. Results: In this review and hypothesis article, based on epithelial-mesenchymal plasticity, especially the hysteresis of epithelial-mesenchymal transition and the hybrid epithelial/mesenchymal phenotype, we proposed a classification of cancer cells, indicating that cancer cells with epithelial-mesenchymal plasticity potential could be classified into four types: irreversible hysteresis, weak hysteresis, strong hysteresis, and hybrid epithelial/mesenchymal phenotype. These four types of cancer cells had varied biology, spreading features, and prognoses. Discussion: Our results highlight that the proposed classification system offers insights into the diverse behaviors of cancer cells, providing implications for cancer aggressiveness and metastasis.

Modular Pelvic Exenteration for Advanced Rectal Cancer in Frozen Pelvis.

BACKGROUND Surgery for locally advanced rectal cancer with frozen pelvis is challenging. Therefore, we designed the "modular pelvic exenteration" surgical strategy to achieve better radical resection. CASE REPORT A 51-year-old man with rectal cancer refused surgery and received chemotherapy and radiotherapy. He was intolerant to chemotherapy and did not respond well to radiotherapy. With cancer progression, he presented at our hospital with emaciation, fatigue, dysuria, bloody urine, bloody stool, and anal pain. Computed tomography and magnetic resonance imaging revealed the rectal tumor involved multiple adjacent organs and caused rectovesical fistula, bilateral hydronephrosis, hydroureterosis, and local pelvic infection. The rectal tumor was fixed in the pelvic cavity, presenting a frozen pelvis pattern. There was no distant metastasis. As the patient could not tolerate chemotherapy, was unsuitable for immune-check point inhibitor because the tumor had microsatellite stability, and did not respond well to radiotherapy, surgical resection seemed the most suitable treatment option. After the patient's anemia and malnutrition improved, our designed modular pelvic exenteration surgery was performed. In this strategy, we divided pelvic organs and tissues into 4 independent modules. After combining the modules planned to be resected, we delineated the pre-resection margin. By this strategy, the tumor was removed en bloc, with a clear resection margin. The patient was discharged 13 days after the operation, without complications. Follow-up for 24 months revealed no signs of tumor recurrence. CONCLUSIONS For locally advanced rectal cancer with frozen pelvis, the modular pelvic exenteration strategy may help to achieve satisfactory surgical effects in selected patients.

A "conversion-deterioration-double mutation" theory for the evolution and progression of colorectal cancer.

In this study, based on some clinical phenomena and recently published knowledge, we proposed our "conversion-deterioration-double mutation" theory, which provides a possible unifying explanation for the evolutionary process of colorectal cancer cells in the human body. In this theory, we proposed that there is a partial interconversion and a jump conversion relationship among normal colorectal epithelial cells, colorectal cancer cells, stem cells, and cancer stem cells (conversion). This conversion leads to tumor heterogeneity. We also proposed that well-differentiated cancer cells converted from cancer stem cells have a more aggressive pattern than primary cancer cells (deterioration). The deterioration of primary cancer cells leads to differences in treatment responses and prognosis. Finally, we speculate a double mutation theory, indicating that for metastasis to occur, both mutations of cancer cells and mutations of target organs are needed and should match and meet. All these three points constitute the "conversion-deterioration-double mutation" theory.

Reconsideration of recurrence and metastasis in colorectal cancer.

To discuss recurrence patterns and their significance in colorectal cancer. Preexisting medical hypotheses and the clinical phenomena of recurrence in colorectal cancer were evaluated and integrated. Colorectal cancer recurrence/metastasis consists of two types: recurrence from the activation of dormant cancer cells and recurrence from postoperative residual cancer cells. These two recurrences have their own unique mechanisms, biological behaviors, responses to therapy, and prognoses. For type 1 recurrences, surgical resection should be considered. Type 2 recurrences should be managed systematically in addition to surgical resection. The two types of colorectal cancer recurrence should be evaluated and managed separately.

Knockdown of SFRS9 Inhibits Progression of Colorectal Cancer Through Triggering Ferroptosis Mediated by GPX4 Reduction.

Ferroptosis, a newly discovered form of programmed cell death characterized by lipid peroxidation, crafts a new perspective on cancer treatment. Serine and arginine rich splicing factor 9 (SFRS9) is frequently described as a proto-oncogene in cervical and bladder cancer. However, the role of SFRS9 in colorectal cancer (CRC) and whether SFRS9 exerts its function associated with ferroptosis is largely unknown. Herein, we found that the expression of SFRS9 mRNA and protein in the CRC tissues was obviously higher than that in the paracancerous tissues. Function assays revealed that SFRS9 overexpression (SFRS9-OE) significantly promoted cell viability, cell cycle progression and colony formation of CRC cells. While SFRS9 knockdown by shRNAs transfection inhibited these progressions. Furthermore, cell death and lipid peroxidation induced by ferroptosis inducers erastin and sorafenib were suppressed by SFRS9-OE. Bioinformatics analysis indicated that SFRS9 can bind to peroxidase 4 (GPX4) mRNA which is a central regulator of ferroptosis. Western blot showed that GPX4 protein expression was clearly elevated upon SFRS9-OE, while it was decreased in SFRS9-inhibited CRC cells. RNA immunoprecipitation experiment was carried out in HCT116 cells to confirm the binding of SFRS9 and GPX4 mRNA specifically. SiGPX4 transfection reversed the inhibitory effects of SFRS9-OE on the erastin and sorafenib-induced ferroptosis. Consistent with our in vitro observations, SFRS9 promoted the growth of tumors while SFRS9 knockdown significantly inhibited tumor growth in nude mice. In conclusion, SFRS9 represents an obstructive factor to ferroptosis by upregulating GPX4 protein expression, and knocking down SFRS9 might be an effective treatment for CRC.

Excising the neovagina due to introital atresia and closed neovaginal loop after sigmoid vaginoplasty: A case report.

INTRODUCTION: Vaginal agenesis is a congenital disorder, which can be managed by nonsurgical dilation or surgical reconstruction of the vagina. The sigmoid vaginoplasty procedure is a popular approach, which pulls down part of the sigmoid colon to form a neovagina. One complication of this procedure is introital stenosis. PATIENT CONCERNS: A 55-year-old woman presented to the outpatient general surgery department with severe, persistent abdominal pain. The patient was diagnosed with congenital absence of uterus and vagina, and a sigmoid vaginoplasty was performed 34 years ago. DIAGNOSIS: A pelvic MRI and an abdominal enhanced CT scan were performed, finding that the uterus was absent, and the os of the vagina was closed, forming a closed loop full of fluid. Introital atresia and closed loop of neovaginal colon conduit were diagnosed. INTERVENTIONS: Based on our conclusions and the patient's consent we surgically removed the neovagina. OUTCOMES: After surgery, the abdominal pain was relieved, and the patient reported full recovery during a 6-month follow-up appointment. CONCLUSION: Introital stenosis is one of the long-term complications of sigmoid vaginoplasty procedure. Introital stenosis, leading to introital atresia, is rare but may occur. Surgical removal of neovagina can relieve the pain in patients who do not have the demand of sexual intercourse.

Inhibition of SRSF9 enhances the sensitivity of colorectal cancer to erastin-induced ferroptosis by reducing glutathione peroxidase 4 expression.

Ferroptosis, a newly iron-dependent form of cell death, is often accompanied by the damage of membrane lipid peroxide. Recently, the ferroptosis inducer erastin has been reported to exhibit potential anti-cancer activities. The aim of this study was to investigate the effects of SRSF9 on the sensitivity of colorectal cancer (CRC) to erastin and explore the underlying molecular mechanism. Short hairpin RNAs (shRNAs) or SRSF9 overexpression vector (SRSF9-OE) was transfected into erastin-induced human CRC cells to inhibit or overexpress SRSF9. Results showed that SRSF9 inhibition promoted the cell death induced by erastin, conversely, SRSF9 overexpression augmented the resistance to erastin-induced death in human CRC cells. SRSF9 decreased lipid peroxide damage which was a key event during erastin-induced ferroptosis in human CRC cells. Furthermore, we found that SRSF9 inhibition increased erastin-induced ferroptosis by downregulating GPX4 level. In an In vivo study, SRSF9 shRNA or SRSF9-OE stably transfected human CRC cells were subcutaneously injected into the right flank of nude mice. SRSF9 overexpression partly abolished the tumor growth inhibition and ferroptosis induced by erastin. Our data indicated SRSF9's regulation of GPX4 as an essential mechanism driving CRC tumorigenesis and resistance of erastin-induced ferroptosis. This molecular mechanism may provide a novel method for improving the sensitivity of CRC to erastin.

Treatment of slow transit constipation-induced ileus during pregnancy by colectomy with ileorectal anastomosis: A case report.

INTRODUCTION: Slow transit constipation is a major cause of chronic constipation. During pregnancy, changes in hormone levels and the physical effects of an enlarged uterus could cause new onset slow transit constipation or aggravate a pre-existing constipation. The management of slow transit constipation-induced ileus during pregnancy is a medical dilemma. PATIENT CONCERNS: A 28-year-old pregnant woman presented to the emergency department with a 7-day history of worsening bloating and abdominal colic. The patient was in her third trimester (27 weeks). She had a 5-year history of constipation which had worsened with her pregnancy, and neither flatus nor stool could be passed. DIAGNOSIS: Based on the constipation history and computed tomography, a slow transit constipation-induced ileus was confirmed. INTERVENTIONS: As medications for the management of constipation and endoscopic efforts to remove the blockage were ineffective and the patient's symptoms worsened, Cesarean section and colectomy with ileorectal anastomosis were performed. OUTCOMES: After the procedure, the patient recovered and defecated well. At the 6-month follow-up, the patient reported that she defecated two to three times per day without difficulty. CONCLUSION: Pregnancy can worsen pre-existing constipation and cause ileus. In cases where drug treatment is unsuccessful, colectomy, and ileorectal anastomosis may be necessary.

MiR-214-3p exacerbates kidney damages and inflammation induced by hyperlipidemic pancreatitis complicated with acute renal injury.

AIMS: Acute pancreatitis (AP) is usually complicated with multiple organ insufficiency, including renal injury. Hyperlipidemia is regarded as a risk factor to induce AP. High-fat diet-induced hyperlipidemic pancreatitis (HP) increased nowadays and showed more severe symptoms and complications than other AP. However, detailed mechanisms or mediators involved in HP complicated with acute renal injury were less studied. Here, we aimed to study how miR-214 expresses in the HP and whether miR-214 has functions to regulate pathological kidney damages induced by HP. MAIN METHODS: Sprague-Dawley rats were adopted to establish HP model complicated with acute renal injury through long-term high-fat diet and sodium taurocholic injection. Models were injected with LV-rno-miR-214-3p or LV-anti-rno-miR-214-3p to exogenously regulate miR-214-3p to study its impacts on HP via a series of molecular and histological experiments. KEY FINDINGS: MiR-214-3p was found to be up-regulated in the kidney, pancreas and serum of HP rats and also could intensify the pathological alterations, kidney and pancreas damages and fibrosis induced by HP. Inflammatory response in HP was enhanced when miR-214-3p was overexpressed. Besides, miR-214-3p up-regulation was showed to inhibit PTEN expression but increased P-Akt levels in the HP kidney, which might be a possible mechanism to induce severe symptoms of pancreatitis. Knockdown of miR-214-3p showed opposite effects. SIGNIFICANCE: MiR-214-3p is indicated to exacerbate the tissue damages and inflammatory response caused by HP complicated with acute renal injury, which may provide a novel therapeutic perspective targeting miR-214-3p to treat HP with acute renal injury.

A novel cancer stem cell-based classification model for the tumorigenesis and development of colorectal cancer.

Cancer is a heterogenetic disease. Although multiple hypotheses and models have been indicated, there is still no robust method to distinguish the heterogeneity of cancer. Evidence has been provided showing that cancer stem cells (CSCs) play an important role in the origin and progression of cancer. In this opinion article, based on the theory of CSCs, we propose a novel CSC-based classification model (CSCCM) to explain the origin and progression of colorectal cancer, which would explain some confusing clinical phenomena and distinguish the heterogeneity of colorectal cancer from its origin. We further suggest that this model can presently be incorporated into the cancer progression theory.

Rectal Mucinous Adenocarcinoma Invading Retrorectal Dermoid Cysts: A Case Report.

Rectal mucinous adenocarcinoma is a subtype of colorectal adenocarcinoma, which is more aggressive and prone to invade adjacent normal organs or tissues compared with non-mucinous adenocarcinoma. Retrorectal dermoid cyst is a rare congenital disease, which usually are benign but with a potential for malignant degeneration. In this article, we report a case which presented a rectal mucinous adenocarcinoma invading into retrorectal dermoid cysts, indicating that besides adjacent normal organs or tissues, malignancies can also invade adjacent tumors, making their diagnosis and management more complicated. In such cases, double primary tumors should be considered, and they should be removed surgically.

The function of BTG3 in colorectal cancer cells and its possible signaling pathway.

PURPOSE: B-cell translocation gene 3 (BTG3) has been identified as a candidate driver gene for various cancers, but its specific role in colorectal cancer (CRC) is poorly understood. We aimed to investigate the relationship between expression of BTG3 and clinicopathological features and prognosis, as well as to explore the effects and the role of a possible BTG3 molecular mechanism on aggressive colorectal cancer behavior. METHODS: BTG3 expression was assessed by immunohistochemistry (IHC) on specimens from 140 patients with CRC. The association of BTG3 expression with clinicopathological features was examined. To confirm the biological role of BTG3 in CRC, two CRC cell lines expressing BTG3 were used and BTG3 expression was knocked down by shRNA. CCK-8, cell cycle, apoptosis, migration, and invasion assays were performed. The influence of BTG3 knockdown was further investigated by genomic microarray to uncover the potential molecular mechanisms underlying BTG3-mediated CRC development and progression. RESULTS: BTG3 was downregulated in colorectal cancer tissues and positively correlated with pathological classification (p = 0.037), depth of invasion (p = 0.016), distant metastasis (p = 0.024), TNM stage (p = 0.007), and overall survival (OS) and disease-free survival (DFS). BTG3 knockdown promoted cell proliferation, migration, invasion, relieved G2 arrest, and inhibited apoptosis in HCT116 and LoVo cells. A genomic microarray analysis showed that numerous tumor-associated signaling pathways and oncogenes were altered by BTG3 knockdown. At the mRNA level, nine genes referred to the extracellular-regulated kinase/mitogen-activated protein kinase pathway were differentially expressed. Western blotting revealed that BTG3 knockdown upregulated PAK2, RPS6KA5, YWHAB, and signal transducer and activator of transcription (STAT)3 protein levels, but downregulated RAP1A, DUSP6, and STAT1 protein expression, which was consistent with the genomic microarray data. CONCLUSIONS: BTG3 expression might contribute to CRC carcinogenesis. BTG3 knockdown might strengthen the aggressive colorectal cancer behavior.

Naringenin induces laxative effects by upregulating the expression levels of c-Kit and SCF, as well as those of aquaporin 3 in mice with loperamide-induced constipation.

Constipation is a common affliction which causes discomfort and affects the quality of life of affected individuals. Naringenin (NAR), a natural flavonoid widely found in citrus fruits and tomatoes, has been reported to exhibit various pharmacological effects, such as anti-inflammatory, anti-atherogenic, anti-mutagenic, hepatoprotective and anticancer effects. Increasing evidence has indicated that NAR has potential for use in the treatment of constipation. Thus, the aim of this study was to evaluate the laxative effects of NAR in mice with loperamide-induced (Lop-induced) constipation. The data indicated that NAR relieved Lop-induced constipation in mice based on the changes of fecal parameters (numbers, weight and water content), the intestinal charcoal transit ratio and the histological alteration. ELISA revealed that NAR regulated the production levels of gastrointestinal metabolic components, such as motilin (MTL), gastrin (Gas), endothelin (ET), substance P (SP), acetylcholinesterase (AChE) and vasoactive intestinal peptide (VIP) in serum. The expression levels of enteric nerve-related factors, glial cell line-derived neurotrophic factor (GDNF), transient receptor potential vanilloid 1 (TRPV1), nitric oxide synthase (NOS), c-Kit, stem cell factor (SCF) and aquaporin 3 (AQP3) were examined by western blot analysis and RT-PCR analysis. The results of this study suggest that NAR relieves Lop-induced constipation by increasing the levels of interstitial cells of Cajal markers (c-Kit and SCF), as well as AQP3. Thus, NAR may be effective as a candidate in patients suffering from lifestyle-induced constipation.

Experimental Quantum Randomness Processing Using Superconducting Qubits.

Coherently manipulating multipartite quantum correlations leads to remarkable advantages in quantum information processing. A fundamental question is whether such quantum advantages persist only by exploiting multipartite correlations, such as entanglement. Recently, Dale, Jennings, and Rudolph negated the question by showing that a randomness processing, quantum Bernoulli factory, using quantum coherence, is strictly more powerful than the one with classical mechanics. In this Letter, focusing on the same scenario, we propose a theoretical protocol that is classically impossible but can be implemented solely using quantum coherence without entanglement. We demonstrate the protocol by exploiting the high-fidelity quantum state preparation and measurement with a superconducting qubit in the circuit quantum electrodynamics architecture and a nearly quantum-limited parametric amplifier. Our experiment shows the advantage of using quantum coherence of a single qubit for information processing even when multipartite correlation is not present.

Rosiglitazone attenuates renal injury caused by hyperlipidemic pancreatitis.

Hyperlipidemic pancreatitis (HP) is a serious inflammatory disease with very high mortality and multiple organ injuries including renal injury. Rosiglitazone (Ros), an agonist of peroxisome proliferator activated receptor-γ (PPAR-γ), was reported to show a protective role against pancreatitis. However, whether Ros has an effect on renal injury caused by HP is not yet clear. In the present study, the function of Ros was explored using ELISA, RT-PCR, western blot, PAS staining and immunohistochemistry. Results of this study showed that Ros could inhibit the activation of NF-κB and MAPK P38 signaling pathways, relieve inflammatory response and inhibit cell apoptosis, thus attenuating renal injury caused by HP. This study suggested that Ros might be a promising drug for the treatment of renal injury caused by HP and also laid theoretical foundation for the development of renal injury treatment.

Overexpression of integrin-linked kinase (ILK) promotes migration and invasion of colorectal cancer cells by inducing epithelial-mesenchymal transition via NF-κB signaling.

Integrin-linked kinase (ILK), a ubiquitously expressed and evolutionally conserved serine/threonine kinase, has been shown to be aberrantly overexpressed and activated in diversified types of human malignancies, including colorectal cancer (CRC). However, the potential role of ILK in cancer cell migration and invasion remains to be elucidated. In this study, we introduced the human ILK gene into a low ILK-expressing human CRC cell line SW480. Cell migration and invasion were evaluated by the wound healing assay and transwell invasion assay, respectively. The epithelial-mesenchymal transition (EMT)-related proteins were detected by Western blot analysis or immunofluorescence. We found that enforced overexpression of ILK in SW480 cells dramatically promoted their migratory and invasive ability in vitro. Furthermore, SW480 cells stably overexpressing ILK underwent EMT, as indicated by mesenchymal morphology, decreased expression of E-cadherin, and increased expression of vimentin, Snail, and Slug. Finally, the nuclear factor (NF)-κB inhibitor BAY 11-7028 or NF-κB p65 small interfering RNA significantly restored the reduced E-cadherin level in ILK-overexpressing cells, suggesting that ILK-mediated down-regulation of E-cadherin is dependent on NF-κB activation. Overall, our study demonstrates a pivotal role of ILK in EMT and metastasis, and suggests novel therapeutic opportunities for the treatment of CRC.

Knockdown of protein phosphatase magnesium-dependent 1 (PPM1D) through lentivirus-mediated RNA silencing inhibits colorectal carcinoma cell proliferation.

Colorectal cancer is one of the most common cancers in the world. Protein phosphatase magnesium-dependent 1 d (PPM1D) is aberrantly upregulated in many human carcinoma cells, and recent research has suggested that it could be a potential therapeutic target of cancer. However, the function of PPM1D in colorectal carcinoma cells is not well studied. To investigate the function of PPM1D in colorectal carcinoma, we used lentivirus-based RNA silencing to knock down the expression of PPM1D in RKO cells. We found that the lentivirus-mediated RNAi system efficiently decreased the expression level of endogenous PPM1D. Inhibiting PPM1D expression efficiently inhibited the proliferation and colony formation of RKO cells. Moreover, we found that PPM1D silencing led to G0/G1 cell-cycle arrest and the accumulation of cells at the sub-G1 phase. Furthermore, we found that PPM1D knockdown reduced the expression level of cyclinB1, inhibited ERK phosphorylation and activated the AKT signaling pathway. We found that PPM1D plays a crucial role in colorectal carcinoma cell proliferation and colony formation. Our work provides strong evidence suggesting that PPM1D is a potential therapeutic target of human colorectal cancers. Lentivirus-mediated PPM1D silencing is a promising gene therapeutic method to treat colorectal cancers.

Mutation spectrum in human colorectal cancers and potential functional relevance.

BACKGROUND: Somatic variants, which occur in the genome of all cells, are well accepted to play a critical role in cancer development, as their accumulation in genes could affect cell proliferations and cell cycle. METHODS: In order to understand the role of somatic mutations in human colorectal cancers, we characterized the mutation spectrum in two colorectal tumor tissues and their matched normal tissues, by analyzing deep-sequenced transcriptome data. RESULTS: We found a higher mutation rate of somatic variants in tumor tissues in comparison with normal tissues, but no trend was observed for mutation properties. By applying a series of stringent filters, we identified 418 genes with tumor specific disruptive somatic variants. Of these genes, three genes in mucin protein family (MUC2, MUC4, and MU12) are of particular interests. It has been reported that the expression of mucin proteins was correlated with the progression of colorectal cancer therefore somatic variants within those genes can interrupt their normal expression and thus contribute to the tumorigenesis. CONCLUSIONS: Our findings provide evidence of the utility of RNA-Seq in mutation screening in cancer studies, and suggest a list of candidate genes for future colorectal cancer diagnosis and treatment.

Expression profile analyses of human HCT-116 colon cancer cell line before and after serum induction.

Multi-exon genes may generate distinct isoforms in different conditions and exhibit versatile properties. Here we investigated the isoform-specific gene expression and the gene expression changes of without and with serum-induced human HCT-116 colon cancer cell lines. For these analyses, 4 transcriptome sequencing datasets were used and 2 replicates for each condition. We observed that ~73% of those expressed genes in four samples generated only one isoform, while ~27% encoded at least two isoforms. Our results show that human gene expression can exhibit great flexibility in alternative splicing. Those expressed genes generated ~1.4 isoforms for each gene across four samples on average. In addition, most of these expressed genes were expressed at moderate or low levels. We found that these four samples have similar patterns of their gene expression distributions. Furthermore, we also conducted the differential expression analysis between without and with serum-induced two conditions of these four samples. We detected that 123 genes were differentially expressed and 110 of them were up-regulated. Among those differentially expressed genes, we found intriguing phenomena that a portion of them could be clustered into different functional groups and some oncogenes and proto-oncogenes are differentially expressed.