BackgroundDistant metastases from follicular thyroid carcinoma are mainly hematogenous and are commonly observed in the lungs and bones. Other rare sites are the parotid gland, skin, brain, ovary, adrenal gland, kidney, pancreas and breast, with chest wall lymph node metastasis being even more rare.Case presentationOver the past 10 years, three surgeries were performed on a 69-year-old women with a history of follicular thyroid cancer and its metastatic lesions. The patient presented with a 3-month history of masses in the left chest. She underwent detailed examination of the chest wall tumors, and surgery was then performed to resect all of the tumors. Based on the histopathology, these lymph nodes were confirmed to harbor metastatic follicular thyroid carcinoma.ConclusionThis study reports the first case of follicular thyroid carcinoma metastasis to the chest wall lymph node.

Breast cancer is a common malignancy in women. Among breast cancer types, triple-negative breast cancer (TNBC) tends to affect younger women, is prone to axillary lymph node, lung, and bone metastases; and has a high recurrence rate. Due to a lack of classic biomarkers, the currently available treatments are surgery and chemotherapy; no targeted standard treatment options are available. Therefore, it is urgent to find a novel and effective therapeutic target. As alteration of ion channels and transporters in normal mammary cells may affect cell growth, resulting in the development and progression of TNBC, ion channels and transporters may be promising new therapeutic targets for TNBC. This review summarizes ion channels and transporters related to TNBC and may provide new tumor biomarkers and help in the development of novel targeted therapies.

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Background: Slc26a9 (Solute carrier family 26 member 9) is a member of Slc26a family of multifunctional anion transporters, which functions as Cl- channel (Liu et al., Front Physiol 2018). Our previous study showed that SLC26A9 deficiency results in the development and progression of gastric cancer, which demonstrated that the key role of SLC26A9 in the tumorigenesis first time (Liu et al., Gastroenterology 2018). However, what’s the role of SLC26A9 in the breast cancer (BC) onset is not clear. We therefore wondered whether Slc26a9 gene is involved in promoting breast carcinogenesis and its mechanisms. Methods: The tissue microarrays and IHC assay were used to detect the expression and clinic relevance of SLC26A9 in the human BC. Different BC cell lines were used to investigate the expression and function of SLC26A9 in the BC. SLC26A9 gene transfect and knockout experiment were performed to detect the regulator role of SLC26A9 in BC cell behaviors. Results: Compared with adjacent normal tissues, SLC26A9 expression was significantly increased in the BC tissue, SLC26A9 expression level in BC correlated with the differentiated state of BC and patient’s clinical outcome, indicating that SLC26A9 may be involved in BC pathogenesis and progression in humans and it might be a novel poor prognosis marker for BC. Moreover, HER2 positive BC tissues exhibited high SLC26A9 expression than HER2 negative BC tissues. Compared with normal mammary cell line, SLC26A9 was significantly upregulated in the all BC cell lines, with highest expression in HER2 enriched cell line SKBR3. Deletion of SLC26A9 in SKBR3 resulted in inhibition of BC cell proliferation, migration and invasion, but promotion of cell apoptosis, which were investigated by different cell function assays, including cell counting Kit-8, cell proliferation curve, Annexin VFITC/PI double staining, Wound-healing and transwell assays respectively. Moreover, SLC26A9 deficiency in SKBR3 caused alteration of epithelial mesenchymal transition (EMT) markers, including downregulation of N-cadherin, Snail1, Fibronectin and Vimentin, but increasement of E-cadherin and ZO-1, accompany with disrupting TGFβ signaling pathways, including downregulation of TGF-β1, p-Smad2 and p-Smad3. However, overexpression of SLC26A9 in SKBR3 resulted in inhibition of cell proliferation, migration and invasion, but promotion of cell apoptosis. Accompanying with activation of TGFβ pathway mediate EMT. Conclusions: Upregulation of SLC26A9 resulted in the development and progression of HER2 positive BC via activation of TGFβ signaling pathways. SLC26A9 might be a novel prognosis marker and therapeutic target for BC. Citation Format: Zhiyuan Ma, Xuemei Liu, Chengli Lu, Jiaxing Zhu, Xiaoming Cheng, Biguang Tuo, Taolang Li. Upregulation of SLC26A9 resulted in the development and progression of HER2 positive breast cancer via activating TGFβ signaling pathway [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS19-27.