Publications by authors named "Dedi Kong"

5 Publications

  • Page 1 of 1

Human Bone Marrow Mesenchymal Stem Cells Modified Hybrid Baculovirus-Adeno-Associated Viral Vectors Targeting I Therapy of Hypopharyngeal Carcinoma.

Hum Gene Ther 2020 Dec 22;31(23-24):1300-1311. Epub 2020 Oct 22.

Departments of Otolaryngology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Hypopharyngeal carcinoma is one of the most aggressive subtypes of squamous cell carcinoma of the head and neck. Although significant progress has been made in surgical techniques, radiotherapy, and chemotherapy, the prognosis is still poor. Mesenchymal stem cells (MSCs) have attracted substantial attention as tumor-targeted cellular carriers for cancer gene therapy. We have previously shown that recombinant baculovirus-adeno-associated vectors (BV-AAV) possessed high efficiency for multi-gene coexpression in human bone marrow MSCs (BMSCs) and BV-AAV-engineered BMSCs could effectively target hypopharyngeal cancer tissues . However, it was not clear whether BV-AAV-engineered BMSCs as cellular vehicles, mediating the expression of the sodium iodide symporter (NIS), would be effective in controlling the growth of hypopharyngeal carcinoma by radioiodine therapy. We constructed a hybrid BV-AAV containing the Luc-P2A-eGFP fusion or NIS sequence to modify BMSCs (BMSCs-Bac-Luc-P2A-eGFP or BMSCs-Bac-NIS). The I uptake of BMSCs-Bac-NIS was analyzed by an automatic gamma counter and micro-single-photon emission computed tomography (SPECT)/computed tomography (CT) imaging . The value of radioiodine therapy for hypopharyngeal carcinoma was evaluated by measuring tumor volume, glucose metabolism (via 2-deoxy-2-[F] glucose [F-FDG] positron emission tomography/CT), and proliferation of tumor cells. We demonstrated that I uptake of BMSCs-Bac-NIS persists over long-term (at least 8 h). Radioactive uptake could be detected by SPECT/CT 1 h after I injection in the BMSCs-Bac-NIS group, showing that this strategy allows for the tracking of real-time migration and transgene expression of BMSCs. Radioiodine therapy resulted in a significant reduction in tumor growth (386.93 ± 249.23 mm vs 816.56 ± 213.87 mm in controls), increased survival, and decreased SUVmax of F-FDG. The hybrid BV-AAV that can provide a variety of genes and regulatory elements, as a novel gene therapy strategy opens the prospect of NIS-mediated radionuclide therapy of hypopharyngeal carcinoma after MSC-mediated gene delivery.
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http://dx.doi.org/10.1089/hum.2020.081DOI Listing
December 2020

Grading system and surgical approaches for endolymphatic sac tumors.

Eur Arch Otorhinolaryngol 2020 Jul 6. Epub 2020 Jul 6.

Department of Otology and Skull Base Surgery, Eye, Ear, Nose, and Throat Hospital, Fudan University, 83 Fenyang Rd, Xuhui District, Shanghai, 200031, People's Republic of China.

Purpose: Endolymphatic sac tumors (ELSTs) are rare, low-grade adenocarcinomas arising from the endolymphatic sac. This study aims to present a novel grading system for ELSTs to determine the optimal management strategy.

Methods: We performed a retrospective analysis of 16 patients with 17 ELSTs. The tumor location and involved adjacent neurovascular structures on CT and MRI were selected to establish the grading system.

Results: Based on the novel grading system, grade III a tumors were most common (7/17), followed by grade I (4/17), grade II (3/17), and grade III b (3/17) tumors. Eight advanced ELSTs (grade III a and III b) received an infra-temporal fossa approach, while the other 6 early stage ELSTs (grade I and II) underwent either a retrolabyrinthine approach with posterior petrosectomy or a translabyrinthine approach combined with subtotal temporal bone resection. Hearing preservation was achieved in 2 grade I patients. Postoperative facial nerve function was HB II in 1 grade III a patient who underwent anterior facial nerve transposition and was HB III in 4 advanced patients who received facial nerve grafts with the great auricular nerve or facial-hypoglossal nerve anastomosis. The mean follow-up time was 35.1 months. Two grade III patients and 1 grade II patient had tumor recurrence during follow-up, among whom 1 grade III b patient had two cases of recurrence.

Conclusion: A correct initial diagnosis was established in all patients after meticulous imaging studies. Surgical resection is still the first choice to manage patients with ELSTs. The novel grading system enables surgeons to select tailored surgical approaches. Long-term follow-up is necessary following surgical intervention.
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http://dx.doi.org/10.1007/s00405-020-06185-3DOI Listing
July 2020

Icariin inhibits cell proliferation, migration and invasion by down-regulation of microRNA-625-3p in thyroid cancer cells.

Biomed Pharmacother 2019 Jan 1;109:2456-2463. Epub 2018 Dec 1.

Department of Thyroid and Breast Surgery, Jining No. 1 People's Hospital, Jining 272011, Shandong, China. Electronic address:

Thyroid cancer (TC) is a familiar cancer, which accounts for approximately 1% of the malignant tumors of all cancers worldwide. Recently, icariin (ICA) has been reported to play an anti-tumor role in different cancers. The study aimed to investigate the effect of ICA on TC cells to uncover the regulatory mechanism. The different concentrations of ICA were stimulated SW579 and TPC1 cells, and cell viability, apoptosis, migration, invasion and main factors of these processes were detected by CCK-8, flow cytometry, Transwell and western blot. The expression of miR-625-3p in TC tissues or in ICA-treated cells was examined by qRT-PCR. MiR-625-3p mimic and the negative control were transfected into SW579 and TPC1 cells to investigate the effect of miR-625-3p on TC. Finally, the signaling pathways of PI3K/AKT and MEK/ERK were examined by western blot. ICA significantly suppressed cell viability in a dose-dependent manner and induced apoptosis by regulating Bcl-2, Bax and cleaced-Caspase-3/-9 expression in SW579 and TPC1 cells (p < 0.001). Moreover, ICA inhibited cell migration and invasion by down-regulating MMP-9 and Vimentin in SW579 and TPC1 cells (p < 0.01 or p < 0.001). The expression level of miR-625-3p was decreased by ICA, and miR-625-3p overexpression reversed the anti-tumor effect of ICA on SW579 and TPC1 cells (p < 0.05, p < 0.01 or p < 0.001). Furthermore, ICA inactivated PI3K/AKT and MEK/ERK signaling pathways by mediating miR-625-3p in SW579 and TPC1 cells. ICA exerted anti-tumor effect by inhibiting cell proliferation, migration and invasion by down-regulating miR-625-3p in TC cells.
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http://dx.doi.org/10.1016/j.biopha.2018.04.012DOI Listing
January 2019

MicroRNA-625-3p promotes the proliferation, migration and invasion of thyroid cancer cells by up-regulating astrocyte elevated gene 1.

Biomed Pharmacother 2018 Jun 22;102:203-211. Epub 2018 Mar 22.

Department of Thyroid Breast Surgery, Jining NO.1 People's Hospital, Jining, 272011, Shandong, China. Electronic address:

Background: Thyroid cancer is the most common malignancy in human endocrine system. This study aimed to investigate the effects of microRNA-625-3p (miR-625-3p) on thyroid cancer cell proliferation, migration, invasion and apoptosis, as well as underlying potential mechanism.

Methods: The relative expressions of miR-625-3p in tumor tissues and adjacent normal tissues of 20 patients with papillary thyroid cancer (PTC) were assessed using qRT-PCR. Cell transfection was used to up-regulate or down-regulate the expressions of miR-625-3p in thyroid cancer SW579 and TPC-1 cells. Effects of miR-625-3p overexpression or suppression on SW579 and TPC-1 cell viability, migration, invasion and apoptosis were detected respectively. The regulatory effect of miR-625-3p on astrocyte elevated gene 1 (AEG-1) expression was also analyzed. Then, the roles of AEG-1 in SW579 and TPC-1 cell proliferation, migration, invasion and apoptosis, as well as Wnt/β-catenin and c-Jun N-terminal kinase (JNK) pathways activation, were evaluated.

Results: miR-625-3p had high expressions in tumor tissues, compared to adjacent normal tissues. Overexpression of miR-625-3p significantly promoted SW579 and TPC-1 cell proliferation, migration and invasion but had no influence on cell apoptosis. Knockdown of miR-625-3p had opposite effects, but induced cell apoptosis. AEG-1 was up-regulated by miR-625-3p overexpression and participated in the effects of miR-625-3p on SW-579 and TPC-1 cells. In addition, overexpression of AEG-1 induced the activation of Wnt/β-catenin and JNK pathways in SW579 and TPC-1 cells.

Conclusion: miR-625-3p promoted proliferation, migration and invasion of thyroid cancer cells by enhancing the expression of AEG-1 and activating downstream Wnt/β-catenin and JNK pathways.
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http://dx.doi.org/10.1016/j.biopha.2018.03.043DOI Listing
June 2018

Association of T-cadherin levels with the response to neoadjuvant chemotherapy in locally advanced breast cancer.

Oncotarget 2017 Feb;8(8):13747-13753

Department of Pharmacy, Jining No.1 People's Hospital, Jiningy 272011, Shandong, People's Republic of China.

Purpose: To examine the association of T-cadherin with pathologic complete response (pCR) after neoadjuvant chemotherapy for locally advanced breast cancer.

Results: T-cadherin expression before and after neoadjuvant chemotherapy was similar (P = 0.162). The multivariable analysis indicated that negative T-cadherin expression was independently associated with pCR after neoadjuvant TAC chemotherapy (P = 0.001).

Materials And Methods: A total of 136 patients with locally advanced breast cancer received four cycles of neoadjuvant TAC chemotherapy (docetaxel + epirubicin + cyclophosphamide), followed by surgery. T-cadherin, estrogen receptor (ER), progesterone receptor (PR), HER-2, and Ki-67 were analyzed by immunohistochemistry. The association between T-cadherin expression and pCR after neoadjuvant chemotherapy was analyzed using multivariable logistic analysis.

Conclusions: Negative T-cadherin expression before and after neoadjuvant chemotherapy for locally advanced breast cancer was similar. T-cadherin could be considered an independent factor associated with the efficacy of such therapy.
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http://dx.doi.org/10.18632/oncotarget.14630DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355134PMC
February 2017