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. 2023 Sep 17;38:101790. doi: 10.1016/j.tranon.2023.101790

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© 2023 The Authors. Published by Elsevier Inc.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig 8 — CAFs promote tumor cell proliferation, invasion, and migration through the SLC38A5-CCL5 axis. (a) The expression of SLC38A5 between NFs and CAFs at both mRNA (left) and protein (right) levels. (b) The efficacy of siRNA targeting SLC38A5 is validated by qRT-PCR (left) and blotting (right). (c) RCC cell lines ACHN (left) and 786-O (right) viability detected by a CCK-8 assay. (d) RCC cells lines ACHN (up) and 786-O (bottom) invasion when co-cultured with CAFs; detected by a transwell assay. (e) RCC cells lines ACHN (bottom) and 786-O (up) migration when co-cultured with CAFs; detected by a wound-healing assay. (f) Heatmap shows the decreased CCL5 expression in si-SLC38A5 CAFs. (g) Correlation between SLC38A5 and CCL5 (GEPIA, http://gepia.cancer-pku.cn/index.html, accessed on 19 December 2022). (h) The de-creased protein level of CCL5 after SLC38A5 inhibition by ELISA. * p < 0.05, ** p < 0.01, *** p < 0.001.