Indian Journal of Cancer
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   2015| December  | Volume 52 | Issue 7  
    Online since July 20, 2016

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MicroRNA-185 is a novel tumor suppressor by negatively modulating the Wnt/β-catenin pathway in human colorectal cancer
W Dong-xu, L Jia, Z Su-juan
December 2015, 52(7):182-185
DOI:10.4103/0019-509X.186576  PMID:27453420
OBJECTIVE: The deregulation of microRNA-185 (miR-185) has been showed to be associated with many cancers and act as a tumor suppressor in many types of human malignancies. We hence tried to find out its role in human colorectal cancer (CRC). MATERIALS AND METHODS: miR-185 expression was investigated by real-time quantitative polymerase chain reaction. We carried out transfections to overexpress or knockdown of miR-185 by mimics or inhibitor, respectively. Functional study like cell counting kit-8 assay was performed to evaluate the proliferation. For addressing the impact of miR-185 on Wnt/β-catenin signaling, we further applied luciferase reporter assay and Western blotting for specific proteins in this pathway. RESULTS: miR-185 was decreased in CRC cell lines when compared with corresponding control cell line. We also proved that its overexpression in LoVo cells could remarkably suppress cell proliferation whereas knocked it down in SW480 cells has the opposite effect in vitro. Mechanically, we demonstrated that miR-185 could suppress the Wnt/β-catenin signaling and modulate the transcription and translation level of downstream molecules of this pathway, including MYC and CCND1. CONCLUSION: Taken together, these results suggested that miR-185 exerts its tumor suppressor activities probably through a negative modulation of the Wnt/β-catenin pathway.
  13 1,845 267
MicroRNA-618 modulates cell growth via targeting PI3K/Akt pathway in human thyroid carcinomas
L Yi, Y Yuan
December 2015, 52(7):186-189
DOI:10.4103/0019-509X.186577  PMID:27453421
OBJECTIVE: MicroRNAs (miRNAs) were popularly investigated in many cancers. The aim of this study was to evaluate the expression, role, and mechanism of microRNA-618 (miR-618) in human thyroid cancer (TC) cells. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction was carried out to examine the expression level of miR-618 in 20 TC tissues with 15 adjacent normal tissues. Synthesized mimics medicated miR-618 overexpression model was done in TC TPC-1 cell line. The effects of cell growth were determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide method. In addition, PI staining followed by flow cytometry was performed to analyze cell cycle. Then, we performed Western blotting to analyze the impact of miR-618 overexpression on the classical PI3K/Akt signaling pathway. RESULTS: We confirmed previous findings that miR-618 was downregulated in TC. Functionally, we found that forced expression of miR-618 suppressed cell proliferation and led to G2/M arrest in TPC-1 cells. Mechanically, we showed that miR-618 overexpression induced a significant inhibition of PI3K/Akt signaling pathway in TPC-1 cells. Importantly, restoration of Akt reversed the growth inhibitory effects of miR-618. CONCLUSION: Taken together, our results described a growth-suppressive role of miR-618 in TC cells partially targeting the PI3K/Akt signaling pathway.
  3 1,798 225
miR-338-3p suppresses epithelial-mesenchymal transition and metastasis in human nonsmall cell lung cancer
W Hong-yuan, C Xiao-ping
December 2015, 52(7):168-171
DOI:10.4103/0019-509X.186569  PMID:27453416
OBJECTIVES: MicroRNAs are important modulators of the cellular epithelial-mesenchymal transition (EMT) process and are associated with metastasis in human nonsmall cell lung cancer (NSCLC). In this study, we tried to investigate the role of miR-338-3p in NSCLC cells. MATERIALS AND METHODS: Real-time polymerase chain reaction was applied to quantify the expression levels of miR-338-3p, as well as EMT-associated molecules in NSCLC cells. Wound healing and transwell assays were performed to evaluate the migration and invasion capacities, respectively. Dual-luciferase reporter assay was finally performed to determine the targeting of zinc finger E-box-binding protein 2 (ZEB2) by miR-338-3p. RESULTS: We found that miR-338-3p was significantly reduced in NSCLC cell lines. Forced expression of miR-338-3p in A549 cells led to the suppression of migration/invasion capacity and inhibition of epithelial markers. In addition, we proved that miR-338-3p could directly target ZEB2. CONCLUSIONS: In general, we summarized that miR-338-3p could inhibit EMT and metastasis of human NSCLC cells, which probably via directly targeting ZEB2 expression.
  3 1,761 299
Receptor for activated protein kinase C 1 suppresses gastric tumor progression through nuclear factor-kB pathway
X Yong-zheng, M Wan-li, M Ji-ming, R Xue-qun
December 2015, 52(7):172-175
DOI:10.4103/0019-509X.186572  PMID:27453417
OBJECTIVE: Nuclear factor-kB (NF-kB) activity is crucial for survival and proliferation of many kinds of malignancies, including gastric cancer (GC). The receptor for activated protein kinase C 1 (RACK1) is known to regulate tumor development, whereas the underlined mechanism has not been described clearly. MATERIALS AND METHODS: We analyzed expression of RACK1 in paired human GC samples by both real-time polymerase chain reaction (PCR) and western blot. Effects of RACK inhibition with small interfering RNA or its overexpression in cultured GC cell lines were evaluated in cell viabilities. NF-kB signaling was investigated using luciferase reporter assay and real-time PCR. RESULTS: RACK1 was significantly decreased in GC samples. Knockdown of RACK elevated GC cell viabilities, whereas overexpression of RACK1 suppressed tumorigenesis of GC cells. Importantly, NF-kB signaling was enhanced after RACK1 expression was inhibited, suggesting the negative regulation of the pro-oncogenic NF-kB activity by RACK1 might contribute to its tumor suppressor role in GC cells. CONCLUSION: Our results support that RACK1 suppresses gastric tumor progression through the NF-kB signaling pathway.
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Upregulated long noncoding RNA SPRY4-IT1 contributes to increased cell viability by activating zinc finger 703 expression in esophageal squamous cell carcinoma
J Xue-Liang, W Ming-Dong, Z Ya-Bi, W Wang-Yue
December 2015, 52(7):164-167
DOI:10.4103/0019-509X.186566  PMID:27453415
OBJECTIVES: The function of long noncoding RNA SPRY4-IT1 in human esophageal squamous cell carcinoma (ESCC) has been showed in the former studies. The purpose of this study was to further analyze the underlined mechanisms responsible for its role in ESCC cells. MATERIALS AND METHODS: Quantitative reverse transcriptase polymerase chain reaction was firstly used to measure the expression of SPRY4-IT1 in 50 ESCC patients of different clinical stages. Loss of function approach was then applied to confirm the biological function, especially cell viabilities in cultured ESCC cells, by cell counting kit-8 and clonogenic assay. We further used western blot to reveal the activation of zinc finger 703 (ZNF703) by SPRY4-IT1. RESULTS: We validated that SPRY4-IT1 was upregulated in ESCC tissues of advanced clinical stages. In vitro function assays demonstrated that SPRY4-IT1 cause promotion of cell viability in ESCC cells. We further verified that SPRY4-IT1 could also activate the expression of ZNF703 in ESCC cells, which might contribute to the role of SPRY4-IT1 in ESCC cells. CONCLUSION: SPRY4-IT1 is a vital regulator in ESCC progression, and the SPRY4-IT1/ZNF703 axis might provide novel clues for future ESCC therapy.
  1 2,006 278
Tashinone II A-sulfoacid-natrum elevates the pain threshold through inhibiting nuclear factor kappa B pathway in neuropathic cancer pain
T Jian-min, L Jun, C Sheng-yang, Y Shuang-mei, C Shu-e, Y Xiu-qin, P Chen, Z Ling-bin
December 2015, 52(7):179-181
DOI:10.4103/0019-509X.186575  PMID:27453419
OBJECTIVE: The purpose of this study was to evaluate the effects of Tashinone II A-sulfoacid-natrum on the pain threshold and potential molecular mechanism for neuropathic cancer pain. METHODS: Forty-five male Balb/c mice were divided into control group model group and experiment group with each 15. The sciatic nerve muscle plexus of experiment and model group were given injection containing S180 sarcoma cell 2 × 10 6 mL for each mouse. Mice in the experiment group were given Tashinone II A-sulfoacid-natrum 25 mg/kg once a day intraperitoneal injection. Moreover, mice in the control group were given physiological saline 25 mg/kg, once a day intraperitoneal injection. The mechanical withdraw threshold and thermal withdraw latency were recorded before S180 sarcoma cell injection and in the time point of day 3, 6, 9, 12, and 14. After 14 days treatment, the mice were treated to death and the sciatic nerve CX3CR1 and nuclear factor kappa B (NF-kB) mRNA was tested by quantitative polymerase chain reaction. RESULTS: Compared with control group, the mechanical and thermal pain threshold of experiment group was significant decreased (P < 0.05). However, compared with the model group, the mechanical, and thermal pain threshold of experiment group was significant elevated in time point of day 3, 6, 9, 12, 14 for mechanical pain threshold and day 9, 12 14 for thermal pain threshold (P < 0.05); the pain threshold for the experiment and model group was decreased in the first 9 days and then elevated gradually. Compared with control group, the CX3CR1 and NF-kB mRNA relative expression in mice sciatic nerve of experiment group was significant elevated (P < 0.05); but compared with model group, the CX3CR1 and NF-kB mRNA relative expression of experiment group was significant decreased (P < 0.05). CONCLUSION: Tashinone II A-sulfoacid-natrum can elevates the mechanical and thermal pain threshold through inhibiting the NF-kB in neuropathic cancer pain rat.
  1 1,469 183
The correlation analysis of primary liver cancer with Type 2 diabetes
Q Su, F Sun, J Li, H Zhang, M Wang, H Zhou, L Qiao
December 2015, 52(7):148-152
DOI:10.4103/0019-509X.186557  PMID:27453412
OBJECTIVE: To explore the relationship between Type 2 diabetes and primary liver cancer. MATERIALS AND METHODS: In the period from December 2008 to December 2014, all blood sugar data of patients in our hospital was collected, and the total number is 18213. Except for repeatedly hospitalized diabetic person, newborn stress status, or venous transfusion blood glucose, gestational diabetes, etc., By retrieving the medical record information of patients in the hospital, and using telephone or letter follow-up the patients, we collected 127 people with type 1 diabetes and found no liver cancer patients; Type 2 diabetes, 10,794 cases of patient information, 59 with primary liver cancer. For data analysis, Stata11.0 ratio was used as the main analysis indicators, using Chi-square test and statistical analysis. RESULTS: About 10,794 Type 2 diabetes cases with 59 primary liver cancer, the incidence is 54.66/10,000, men liver cancer incidence (92.78/10,000) than women (27.13/10,000), with significant difference (χ2 = 26.621, P < 0.001). As the growth of the age, the possibility of liver cancer in patients with diabetes increased significantly (χ2 = 19.961, P = 0.001). The rate was highest for 50-60-year-old men, and the women at age 70, and older incidence is highest. Irrespective of men or women with diabetes as the growth of the age, the possibility of liver cancer had significantly increased (P = 0.001, P = 0.002). Hepatitis B or hepatitis C incidence was 2.94%, but diabetes incidence of hepatitis men (3.98%) and women (2.01%) did not find significant differences (χ2 = 0.3361, P = 0.562). Three hundred and seventeen cases of Type 2 diabetes with hepatitis, the incidence of primary liver cancer was 11.67%, the liver cancer incidence of diabetes patients with hepatitis men (17.78%) than women (3.97%), with significant difference (χ2 = 37.429, P < 0.001). With the growth of age, the overall risk of getting liver cancer (χ2 =15.023, P = 0.01) of diabetes and hepatitis patients is significantly increased, and with the growth of age, the risk of getting liver cancer of male patients showed significant (P < 0.05), but not the female patients. Without merge hepatitis, the morbility of primary liver cancer in 10477 cases of type2 diabetes incidence is 0.21%, the liver cancer incidence men (0.34%) than women (0.11%), with significant difference (χ2 = 6.471, P = 0.011).As the growth of age, the overall risk of getting liver cancer of diabetes patients without hepatits is significantly increased (χ2 =15.612, P = 0.008) ,and the risk of getting liver cancer of male patients showed significant (P < 0.05) as the growth of the age, but not the female patients. Diabetic persons according to the illness time can be divided into 0-5 years, 5-10 years, 10-20 years, and over 20 years of four stages, including 5-10 years and 10-20 years is liver cancer patients with diabetes incidence peak, male diabetic hepatitis in patients with liver cancer incidence than women, with significant difference (χ2 = 22.757, P < 0.001). The possibility of liver cancer in patients with diabetes increased significantly (χ2 = 15.023, P = 0.01) for longer duration of illness, but only the male patients with liver cancer incidence showed significant difference with longer duration of illness, women showed no significance. CONCLUSION: Diabetes was associated with the primary liver cancer, most likely is one of the causes of primary liver cancer.
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Long noncoding ribonucleic acids maternally expressed gene 3 inhibits lung cancer tumor progression through downregulation of MYC
L Yan-hua, L Xiang-lei, L Hong, W Jian-jun
December 2015, 52(7):190-193
DOI:10.4103/0019-509X.186579  PMID:27453422
OBJECTIVE: Long noncoding ribonucleic acids (RNAs) nowadays emerge as important biomarkers or potential therapeutic targets discussed in human cancers. Among them, maternally expressed gene 3 (MEG3) is known to be decreased in a variety of malignancies. MATERIALS AND METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to detect the expression of MEG3 in forty pairs of lung cancer (LC) tissues. Overexpression of MEG3 was carried out, and we determined its effect on cell proliferation, apoptosis, and migration evaluated by cell counting kit-8, flow cytometric, and transwell analysis. Messenger RNA and protein expression of MYC were determined by qRT-PCR and western blot, respectively. RESULTS: The expression of MEG3 was downregulated in LC tissues. Forced expression of MEG3 led to reduced abilities of cell proliferation and elevated apoptosis rate. It also slightly inhibited cell migration capacity in vitro. In addition, MYC was inhibited by MEG3 overexpression at both transcriptional and translational levels. CONCLUSION: Our findings revealed MEG3 could regulate LC progression and serve as an important target for LC treatment.
  1 1,907 348
Superiority of ultrasound-guided over conventional transbronchial needle aspiration in biopsy of lymph nodes: Have we had sufficient evidence?
Q Liu, R Wang, G Zeng
December 2015, 52(7):141-143
DOI:10.4103/0019-509X.186553  PMID:27453410
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Prognostic role of s-phase kinase-associated protein 2 in breast cancer: A meta-analysis
Y Shi, N Li, H Ren, X Guo, Q Li, S Ma, D Wang
December 2015, 52(7):153-157
DOI:10.4103/0019-509X.186559  PMID:27453413
OBJECTIVE: Emerging evidence has shown that the F-box protein S-phase kinase-associated protein 2 (Skp2) plays an important role in the pathogenesis of breast cancer (BC). Our study aimed to evaluate the prognostic value of Skp2 in BC patients using meta-analysis based on the published studies. MATERIALS AND METHODS: Eligible studies were identified by searching the online databases such as PubMed, EMBASE, and Web of Science up to October 2015. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated to clarify the correlation between Skp2 expression and indicators of BC clinical outcomes, including overall survival (OS), disease-free survival (DFS), and BC-specific survival. RESULTS: In total, nine studies with 1820 BC patients were included for final analysis. The meta-analysis suggested that Skp2 overexpression was associated with poor OS (HR = 2.58, 95% CI: 1.83-3.63, P = 0.000) and poor DFS (HR = 2.12, 95% CI: 1.48-3.05, P = 0.000) in BC patients. CONCLUSIONS: This meta-analysis indicates that enhanced Skp2 is an independent prognostic factor for poor cancer survival.
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High preoperative and postoperative levels of carcinoembryonic antigen and CYFRA 21-1 indicate poor prognosis in patients with pathological Stage I nonsmall cell lung cancer
X Duan, Y Cui, H Li, G Shi, B Wu, M Liu, D Chang, T Wang, Y Kong
December 2015, 52(7):158-163
DOI:10.4103/0019-509X.186564  PMID:27453414
BACKGROUND: Serum carcinoembryonic antigen (CEA) and the soluble fragment of cytokeratin 19 (CYFRA 21-1) are supposed to have a prognostic role in patients with nonsmall cell lung cancer (NSCLC) after surgery, but it has not been used as an adjunct to the tumor-node-metastasis (TNM) staging system to provide therapy options for patients with pathological Stage I NSCLC. This study was designed to investigate the effect of serum levels of CEA and CYFRA 21-1 before and after surgery on the prognosis of patients with Stage I NSCLC. MATERIALS AND METHODS: A retrospective review was performed regarding the medical records and follow-ups of 169 patients with Stage I NSCLC before and after surgery. The patients were divided into three groups based on levels of serum CEA and CYFRA 21-1 before and after surgery: (1) continuously normal-level groups (CEA [NN] and CYFRA 21-1 [NN] groups); (2) declined to normal-level groups (CEA [HN] and CYFRA 21-1 [HN] groups); and (3) continuously high-level groups (CEA [HH] and CYFRA 21-1 [HH] groups). Survival analysis was conducted using the Kaplan-Meier method for each group. The Chi-square or Fisher exact test was employed to compare clinical and pathologic factors at the level of P < 0.05. The prognostic factor was evaluated by the Cox proportional hazards model. RESULTS: Compared with the continuously normal-level groups, the CEA [HN] group was significantly correlated to tumor size (P = 0.011), and the CYFRA 21-1 [HN] group was significantly correlated to tumor type and pathological TNM in addition to tumor size. Five-year survivals were significantly lower (P = 0.004) in the CEA [HH] group (67.3%) and the CEA [HN] group (86.5%) than in the CEA [NN] group (85.7%) and were significantly lower (P < 0.001) in the CYFRA 21-1 [HH] group (47.2%) and the CYFRA 21-1 [HN] group (70.1%) than in the CYFRA 21-1 [NN] group (90.1%). Multivariate analysis demonstrated that tumor size (21-50 mm), CEA [HH], and CYFRA 21-1 [HH] were independent unfavorable prognostic factors for overall survival (OS), whereas tumor size (21-50 mm), CEA [HH], CYFRA 21-1 [HN], and CYFRA 21-1 [HH] were independent significant prognostic factors for progression-free survival (PFS). CONCLUSION: Patients with a persistently high serum CEA or CYFRA 21-1 before and after surgery had shortest OS and PFS. These patients had worst prognosis. Adjuvant chemotherapy was likely to improve survival for these patients.
  - 1,977 321
Programmed cell death 1 expression in esophageal squamous cell carcinoma and association with clinical characteristics
Z Feng, Li Xiang-lei, W Hai-tao, W Zuo-pei, H Bao-li, Z Hai-feng, W Xiao-long, L Li
December 2015, 52(7):176-178
DOI:10.4103/0019-509X.186574  PMID:27453418
OBJECTIVE: The aim of this retrospective study was to evaluate the programmed cell death 1 (PD-1) expression in esophageal squamous cell carcinoma (ESCC) and association with clinical characteristics. MATERIALS AND METHODS: From January 2009 to December 2014, 88 patients with ESCC were retrospectively included in this study. Eighty-eight cancer tissues, 35 paraneoplastic atypical hyperplasia tissues (PAHTs), and 30 relative normal esophageal tissues (RNETs) were collected and tested for expression of PD-1 by immunohistochemistry assay. The PD-1 expression and clinical characteristics of the ESCC patients were evaluated. The prognosis of the ESCC patients was compared between the PD-1 positive and negative patients. RESULTS: The PD-1 positive rate was 51.2% (45/88), 22.9% (8/35), and 6.7% (2/30) for the cancer tissue, PAHT, and RNET, respectively, with statistical difference (P < 0.05); The PD-1 expression was significantly associated with lymph node metastasis (P < 0.05) and pathology grade (P < 0.05). The median overall survival was 29.8 months and 32.1 months for the PD-1 positive and negative groups without statistical difference (hazard ratio = 1.00, 95% confidence interval = 0.58-1.71, P < 0.05). CONCLUSION: PD-1 may play a key role in the process of carcinogenesis of ESCC but not associated with prognosis and overall survival.
  - 1,766 294
The role of ppGalNAc-T family in breast cancer development and progression
R Yang, H Zhang, Y Ma, S Gong, J Niu, J Ma, A Zhong
December 2015, 52(7):144-147
DOI:10.4103/0019-509X.186556  PMID:27453411
Glycosylation of proteins is an essential process in all eukaryotes. Mucin-type O-linked glycosylation is an evolutionarily conserved protein modification as a kind of glycosylation of proteins. The role of O-glycosylation was well documented in multiple cancers. While in breast cancer, the enzymes that catalyzed the initiation of O-glycosylation remained elusive. In this review, we briefly introduced the process of the initiation of O-glycosylation and summarized the roles of enzymes that catalyzed the initiation step of O-glycosylation in the breast cancer carcinogenesis, development, and progression. Finally, we summarized some attempts exploring the therapy against aberrant O-glycosylation.
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