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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to <t>lncRNA</t> <t>microarray</t> analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.
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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to <t>lncRNA</t> <t>microarray</t> analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.
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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to <t>lncRNA</t> <t>microarray</t> analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.
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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to <t>lncRNA</t> <t>microarray</t> analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.
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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to <t>lncRNA</t> <t>microarray</t> analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.
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Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to lncRNA microarray analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Unveiling the role of the KLF4/Lnc18q22.2/ULBP3 axis in the tumorigenesis and immune escape of hepatocellular carcinoma under hypoxic condition

doi: 10.1111/jcmm.18411

Figure Lengend Snippet: Lnc18q22.2 is upregulated in hypoxia induced HCC cells. (A, B) SMMC7721 and Hep3B cells were cultured under normoxic and hypoxic conditions and then subjected to lncRNA microarray analysis. (C) The top eight significantly upregulated lncRNAs were listed as indicated. (D, E) HCC cells were subjected to treatment under hypoxic/normoxic, Lnc18q22.2 was measured at different time poinst as indicated. (F, G) HCC cells were exposed to 100 μM CoCl2 with different concentrations 8 h, Lnc18q22.2 was measured as indicated. (H, I) the subcellular distribution of Lnc18q22.2 in HCC cells was validated. (J, K) SMMC7721 cells underwent transfection with si‐NC and si‐HIF‐1α. Following a 24‐h transfection period, cells were cultured under either normoxic or hypoxic conditions for an additional 24 h. The expression levels of HIF‐1α were assessed through western blot analysis, while the levels of Lnc18q22.2 expression were determined using qRT‐PCR. (L, M) SMMC7721 cells were transfected with pcDNA3.1‐HIF‐1α. After a 24‐h transfection period, the expression level of HIF‐1α was assessed through western blot analysis. Concurrently, the levels of Lnc18q22.2 expression were examined using qRT‐PCR. The results were presented as mean ± SD with a sample size of n = 3.

Article Snippet: The microarray was subsequently analysed using the Arraystar lncRNA Microarray and scanned with the Agilent G2505C Scanner.

Techniques: Cell Culture, Microarray, Transfection, Expressing, Western Blot, Quantitative RT-PCR