Cancer Research and Treatment

Original Articles

Apoptosis and Expression of AQP5 and TGF-β in the Irradiated Rat Submandibular Gland: Jin Hwa Choi, Hong-Gyun Wu, Kyeong Cheon Jung, Seung Hee Lee, Eun Kyung Kwon; Cancer Res Treat. 2009;41(3):145-154. Published online September 28, 2009; DOI: https://doi.org/10.4143/crt.2009.41.3.145

Purpose

To evaluate the effect of X-ray irradiation on apoptosis and change of expression of aquaporin 5 (AQP5) and transforming growth factor-β(TGF-β) in the rat submandibular gland (SMG).

Materials and Methods

SMGs of 120 male Sprague-Dawley rats were irradiated with a single X-ray dose (3, 10, 20, or 30 Gy). At the early and late post-irradiation phase, apoptosis was measured by the terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) method, and expression of AQP5 and TGF-β was determined by immunohistochemical staining.

Results

At the late post-irradiation phase, increased apoptosis was evident and marked decreases of expression of AQP5 expression by acinar cells and TGF-β expression by ductal cells were evident.

Conclusion

Apoptosis after X-ray irradiation develops relatively late in rat SMG. Irradiation reduces AQP5 and TGF-β expression in different SMG cell types.

Citations

Citations to this article as recorded by

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Priyanka Chowdhury, Anastasia Velalopoulou, Ioannis I. Verginadis, George Morcos, Phoebe E. Loo, Michele M. Kim, Seyyedeh Azar Oliaei Motlagh, Khayrullo Shoniyozov, Eric S. Diffenderfer, Emilio A. Ocampo, Mary Putt, Charles-Antoine Assenmacher, Enrico Rad
Molecular Cancer Therapeutics.2024; 23(6): 877. CrossRef
A single dose of radiation elicits comparable acute salivary gland injury to fractionated radiation
Amanda L. Johnson, Sonia S. Elder, John G. McKendrick, Lizi M. Hegarty, Ella Mercer, Elaine Emmerson
Disease Models & Mechanisms.2024;[Epub] CrossRef
Oxidative‐antioxidant imbalance in chronic sialadenitis of submandibular gland in human and rat
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Noninvasive Monitoring of Radiation-Induced Salivary Gland Vascular Injury
E.R. Bolookat, L.J. Rich, V.K. Vincent-Chong, C.R. DeJohn, M. Merzianu, P.A. Hershberger, A.K. Singh, M. Seshadri
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Insights into the Function of Aquaporins in Gastrointestinal Fluid Absorption and Secretion in Health and Disease
Giuseppe Calamita, Christine Delporte
Cells.2023; 12(17): 2170. CrossRef
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The Expression of TGF-beta1 and TGF-beta2 in Prostatic Carcinoma: Ki Kwon Kim, Jung Ran Kim, Dong Hoon Kim, Tae Jung Jang, Jong Im Lee, Kyung Sub Lee; J Korean Cancer Assoc. 1998;30(5):970-979.

Abstract PDF: Transfonning growth factor-beta (TGP-beta) is a multipotent growth factor affecting development, homeostasis, and tissue repair. We evaluate the significance of the expression of TGF-beta1 and TGF-beta2 and correlation with prognostic factors in prostate cancer.
MATERIALS AND METHODS
In order to investigate the expression of TGF-beta1 and TGF-beta2, we analyzed Immunohistochemical staining from paraffin blocks of 22 cases of the prostate carcinoma and adjacent normal prostate.
RESULTS
The expressions of TGF-beta1 and TGF-beta2 were noted in the cytoplasm of tumor cells, normal epithelial cells and stroma. The staining intensity and areas were examined and scored from 0 to 5. The TGF-beta1 staining scores of the tumor cells were higher than that of the adjacent normal epithelial cells (p=0.001). The TGF-beta2 staining scores of the tumor cells were also higher than that of the adjacent normal epithelial cells (p=0.003). However, there were no correlation between tumor surrounding stroma and normal stroma in TGF-beta1 and TGF-beta2 staining scores. The serum PSA level, the clinical stage, the Gleason score and the lymph node metastasis of the tumor did not correlated with the staining score of TGF-beta1 and TGF-beta2.
CONCLUSION
These results indicate that the prostatic cancer was associated with alteration of TGF-beta1 and TGF-beta2 expression by prostatic epithelial cells which play a role in prostatic carcinogenesis.

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Plasma TGF-beta1 as a Tumor Marker in Breast Cancer Patients: Hwa Young Lee, Sun Young Rah, Soo Jung Gong, Joong Bae Ahn, Kwang Yong Shim, Joon Oh Park, Hyun Ja Kwon, Nae Choon Yoo, Sook Jung Jeong, Hyun Cheol Chung, Joo Hang Kim, Kyong Sik Lee, Jin Sik Min, Byung Soo Kim, Jae Kyung Roh; J Korean Cancer Assoc. 1998;30(5):935-942.

Abstract PDF: PURPOSE
Transforming Growth Factor-beta1(TGF-beta1) is the most potent inhibitor of the progression of normal mammary epithelial cells through the cell cycle. However, advanced breast cancers are mostly refractory to TGF-beta mediated growth inhibition and produce large amounts of TGF-beta, which may enhance tumor cell invasion and metastasis by its effects on extracellular matrix. Yet, little is known about the association of TGF-beta1 with progression of malignant disease in vivo. In this study, we evaluated the preoperative and postoperative plama level of TGF- in breast cancer and analyzed the utility of plasma TGF-beta1 as possible tumor marker.
MATERIALS AND METHODS
ELISA(enzyme-linked immunosorbent assay) was used to measure plasma TGF-beta1 level in 45 newly diagnosed breast cancer patients and in 15 normal healthy people, and the results were compared with clinicopathologic characteristics.
RESULTS
The mean plasma TGF-beta1 levels were 1.73+/-0.47 ng/ml in normal people and 5.05+/-1.41 ng/ml in breast cancer patiens. In 37 operated patients, the preoperative plasma TGF-beta1 level was 6.34+/-1.34 ng/ml and decreased to 4.48+/-1.07 ng/ml in patients with follow-up after surgery and 4.74+/-0.79 ng/ml in patients with chemotherapy. However, there was no significant correlation between plasma TGF-beta1 level and known prognostic factors including tumor size, LN involvement, tumor grade, hormone receptor status, and pathology.
CONCLUSION
These findings suggest that the plasma TGF-g level can be a tumor marker in breast cancer patients and the association with progression of breast cancer will be explored in future studies.

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Microsatellite Instability Correlate with a Prognosis in Breast Cancer: Hwa Young Lee, Chengshi Quan, Soo Jung Gong, Joon Oh Park, Joong Bae Ahn, Kwang Yong Shim, Sun Young Rha, Nae Choon Yoo, Woo Ick Yang, Joo Hang Kim, Jae Kyung Roh, Kyong Sik Lee, Byung Soo Kim, Hyun Cheol Chung; J Korean Cancer Assoc. 1998;30(5):914-920.

Abstract PDF: PURPOSE
Microsatellite instability in patients with defects in the mismatch repair system resulting in RER has a high risk of accumulating mutations in oncogene and tumor suppressor gene. In this study, we evaluated the incidence of microsatellite instability in breast cancer by comparing PCR-amplified sequences from frozen samples of normal and tumor tissue fram affected patients. We also investigated whether RER was associated with TGF-beta RII mutation.
MATERIALS AND METHODS
Fifty surgically resected breast cancer specimens from Jan. 1996 to June, 1997 were used for study. Microsatellite instability(referred to as replication error, RER) at three loci with BAT 26, BAT 40, TA10 was analyzed by polymerase chain reaction and the results were compared with clinicopathologic characteristics.
RESULTS
Of the 50 breast cancer patients, 14(28%) were RER(+) at one or more microsatellite loci, and 4(8%) showed TGF-beta RII mutation. Microsatellite instability was significantly correlated with lymph node involvement(especially in case of 4 or more lymph nodes involvement). But we could not find any correlation between RER and other prognostic factors including tumor size, tumor grade, hormone receptor status and pathology. One of fourteen tumors with RER(+) showed TGF-beta RII mutstion. There was no signiticant correlation between RER(+) and TGF-beta type II receptor gene mutation.
CONCLUSION
The findings suggest that microsatellite instability would be useful prognostic factor in unilateral breast cancer patients, and the role of targeting to gene mutation will be explored in future studies.

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TGF-beta-1 Expression and p53 Mutation in Non-small Cell Carcinomas of the Lung: Han Kyeom Kim, Seol Hee Park, Young Soon Na, Yong Gu Kang, Young Sik Kim, Jung Ho Han, Mee Ja Park, Insun Kim; J Korean Cancer Assoc. 1997;29(6):1022-1031.

Abstract PDF: PURPOSE
TGF-beta-1 is actually a major growth inhibitor for most cell types. We assumed that the loss of TGF-beta-1 would be occurred during carcinogenesis of the lung. Also, the mutation and expression of p53 have been known to be major moleclar change of non-small cell carcinoma of the lung. So, the relationship between the mutation of p53 and the expression of TGF-beta-1 in the non-small cell carcinomas were evaluated.
MATERIALS AND METHODS
In 43 non-small cell carcinoma and normal tissue of the lung, their TGF-beta-1 mRNA were measured by RT-PCR and p53 was studied by SSCP and Western blotting assay.
RESULTS
p53 mutation rate in non-small cell carcinomas of the lung (48.4%) was much more frequent than the normal control group (14.3%). The expression rate of TGF-beta-1 in lung carcinomas, especially squamous cell carcinoma (71.4%), was much higher than the normal control group (42.9%). p53 mutation and TGF-beta-1 mRNA in the lung carcinomas were not strongly correlated.
CONCLUSION
It suggests that high expression rate of TGF-beta-1 and p53 mutation are associated with carcinogenesis of non-small cell carcinoma of the lung. High expression rate of TGF-beta-1 in the lung carcinomas can be partly explained by the fact that TGF-beta-1 have capacity to control the production of many components of the extracellular matrix and enhance angiogenesis in favor of tumor growth despite of their inhibitory effects of cell growth. However, additional research is required to determine the exact role of TGF-beta-1 in carcinogenesis of the lung.

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